Comprehensive Physiology Wiley Online Library

Memory: Neural Organization and Behavior

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Definitions: From Synapses to Behavior
2 What is Memory? Neurobiological Questions
2.1 The Nature of Synaptic Change
2.2 Neurons Versus Synapses
2.3 Competition
2.4 Remembering and Forgetting
3 What is Memory? Neuropsychological Questions
3.1 Memory Determined by Information Processing
3.2 A Taxonomy of Memory
3.3 Summary
4 Where is Memory?
4.1 Two Historical Views: Localized Versus Distributed Memory
4.2 Locating the Engram
4.3 Summary
5 How is memory organized?
5.1 Modulation of Memory by Neurotransmitters and Hormones
5.2 Amnesia: A Selective Clinical Syndrome
5.3 Amnesia as a Window on Normal Function
5.4 Prefrontal Cortex
5.5 Specific Events Versus Cumulative Experience
5.6 Summary
Figure 1. Figure 1.

Diagram of a synapse onto a dendritic spine showing measures of synaptic morphology that have been used to study experience‐dependent structural alterations at synapses. Experience can also increase the number of synapses, presumably either by forming them outright or by selectively preserving some synapses from a population that is continuously being replaced.

From Chang and Greenough
Figure 2. Figure 2.

Morphological plasticity of synapses dependent on behavioral experience (top) or longterm potentiation (LTP) in hippocampus (bottom). Top: densities of synapses and neuronal nuclei were determined in upper occipital cortex (layers I‐IV), and these values were used to derive an estimate of the number of synapses per neuron. Rats were reared from 23 to 55 days of age in a complex environment (EC), in pairs in social cages (SC), or in individual cages (IC). Enriched rearing conditions resulted in an increased number of synapses per neuron. Neuronal density was decreased in EC animals because of a greater volume of neuronal somata, neuronal processes, and glia. Bottom: brief bursts of high‐frequency stimulation (100 Hz for 1 s or 200 Hz for 0.5 s) produced LTP of the Schaffer collateral‐CA1 system in rat. In the CA1 zone, LTP increased the number of synapses on the dendritic shafts (A) and the number of sessile spine synapses (B). Density of the much more common spine synapse was not affected.

From Greenough
Figure 3. Figure 3.

Three events in the development of specific connections in the vertebrate nervous system: cell death, axon collateral elimination, and synapse elimination. It is estimated that 50% of the nerve cells that are initially formed die before postnatal life. Process elimination by the surviving neurons involves both the removal of whole pathways and the elimination of functional synapses within remaining pathways. In this way, specific connections and networks are sculpted out of the initially formed nervous system.

From Cowan and O'Leary
Figure 4. Figure 4.

Pattern of arborization of a single geniculocortical afferent in the visual cortex of a 17‐day‐old kitten (left) and an adult cat (right). Prior to the segregation of cortical inputs into alternating left‐eye and right‐eye columns, the aborization of individual afferents extends uniformly over a disk‐shaped area >2 mm in diameter. This area is destined to be segregated into at least 4 columns. In the adult, after column formation is complete, individual afferents do not aborize uniformly. The arborization is divided into a number of clumps separated by gaps whose dimensions correspond to the size of individual ocular dominance columns. The gaps are filled with afferents serving the other eye.

From LeVay and Stryker
Figure 5. Figure 5.

Top left: ocular‐dominance distribution of 223 cells recorded from striate cortex of normal adult cats. Cells in groups 1 and 7 could be driven by only one eye. In groups 2, 3, 5, and 6, cells were driven better by one eye than the other. In group 4, cells were driven about equally by each eye. Bottom: ocular‐dominance distribution of 34 cells recorded from the left and right striate cortex of a cat without visual experience in the right eye from 9 wk to 6 mo of age. Majority of cells responded only to visual stimulation from the experienced eye. Top right: ocular‐dominance distribution of 126 cells recorded from cats without visual experience in either eye from ∼1 wk to ∼3 mo of age. Thirty‐seven cells did not respond to visual stimulation. In contrast to the effects of unilateral eye closure, after bilateral eye closure both eyes could drive cortical cells.

Adapted from Wiesel and Hubel
Figure 6. Figure 6.

Summary of cortical visual areas and their known connections. There are 2 major routes from striate cortex (V1): one follows a ventral route into the temporal lobe via area V4 and the other follows a dorsal route into the parietal lobe via MT. Filled arrowheads indicate “forward” projections; arrowheads indicate “backward” projections; lines with filled arrowheads at both ends indicate “intermediate” projections; d indicates that the projection is limited to the dorsal portion of the area; m indicates that it is limited to the medial portion. Other potential pathways into the parietal lobe include those carrying input from the peripheral visual field (dotted lines).

From Ungerleider and Desimone
Figure 7. Figure 7.

Recognition performance on the delayed nonmatching‐to‐sample test. Left: monkeys see an object and then 10 s later must choose the novel, unfamiliar object. Different objects are used on every trial. Right: performance by groups with bilateral lesions of posterior temporal cortex (TEO) or anterior temporal cortex (TE) and a group of unoperated controls (N). Numbers to the left of the curves are average numbers of trials needed after surgery to relearn the basic task, which involved remembering a single object for 10 s. First point on the curve is the average final score in this condition. Animals were subsequently tested in the same task with delay gradually increased from 10 s to 120 s.

Adapted from Mishkin
Figure 8. Figure 8.

A chess‐specific memory skill. Left: board position after the 25th move of Game 6 of the 1984 World Chess Championship in Moscow between A. Karpov (black) and G. Kasparov (white). Right: a random arrangement of the same 19 pieces. After briefly viewing the board of a real game, master players can reconstruct the board from memory much better than weaker players. With a randomly arranged board, experts and beginners perform the same.

See Chase and Simon for details
Figure 9. Figure 9.

Acquisition of a memory skill. In 20 mo involving ∼190 h of practice (1 h/day, 3–5 days/wk), a college student increased his digit span from 7 to 79 digits. Random digits were read to him at the rate of 1/s. If a sequence was recalled correctly, 1 digit was added to the next sequence.

From Ericsson et al. . Copyright 1980 by the American Association for the Advancement of Science
Figure 10. Figure 10.

Extended digit span. Five amnesic patients (including patient HM) and 20 control subjects were read a sequence of 5 digits. If the sequence was repeated back correctly, 1 digit was added to the next sequence; if not, the same sequence was given until it was repeated correctly. Amnesic patients had a normal digit span but required an abnormal number of trials to learn supraspan strings of digits. No amnesic patient recalled more than 12 digits within the testing limit of 25 trials.

From Drachman and Arbit . Copyright 1966, American Medical Association
Figure 11. Figure 11.

Serial‐position curves for 6 amnesic patients and 6 control subjects. Subjects were read 10‐word lists and then asked to recall them in any order. Percentage of items recalled is plotted as a function of their position in the list. Amnesic patients show the normal recency effect but an impaired primacy effect.

From Baddeley and Warrington
Figure 12. Figure 12.

Serial‐position curves for normal rats and rats with hippocampal lesions. Rats first visited 8 arms of a radial maze in a fixed sequence; 20 s (no delay) or 30 min (delay) later they were given a choice test involving arms 1 vs. 2, 4 vs. 5, or 7 vs. 8. They were rewarded for entering the arm that they had visited earlier. A: performance of normal animals showing both a primacy and recency effect in the no‐delay condition. B: performance of normal and operated animals in the no‐delay condition. C: performance of operated animals in the no‐delay and delay conditions.

From Kesner and Novak . Copyright 1982 by the American Association for the Advancement of Science
Figure 13. Figure 13.

Acquisition and retention of a mirror‐reading skill despite amnesia for the learning experience. A: patients prescribed bilateral (BIL) or right unilateral (RUL) electroconvulsive therapy and depressed patients (DEP) not receiving electroconvulsive therapy practiced mirror reading during 3 sessions (50 trials/session). For the patients receiving electroconvulsive therapy, 1 treatment intervened between the first 2 sessions, and an average of 7 treatments intervened between the second and third sessions. B: at the beginning of the third session, subjects were tested for their recollection of the previous testing sessions (9‐point interview) and for their memory of the words they had read (recognition test, chance = 50%).

From Squire et al. . Copyright 1984, Pergamon Press
Figure 14. Figure 14.

Intact priming in amnesia. Amnesic patients and control subjects saw common words and then were asked to recall the words (free recall) or were cued with the first 3 letters of the words and asked to recall them (cued recall). Amnesic patients were impaired in these 2 conditions but performed normally when they were given the first 3 letters of words and instructed simply to form the first word that came to mind (completion). Base‐line guessing rates in the word completion condition were 9%.

From Graf et al. . Copyright 1984 by the American Psychological Association. Reprinted by permission
Figure 15. Figure 15.

Diminution of priming effects across modality. Amnesic patients (AMN), alcoholic control subjects (ALC), and medical inpatients (INPT) read or heard words and then were cued visually with the first 3 letters of these words and asked to form the first words that came to mind. Priming was equivalent across groups and was higher when the study words and the test cues were in the same modality (right). (Hatching shows base‐line word‐completion performance when the words were not presented for study.) Amnesic patients were markedly impaired at recalling words, and recall was unaffected by the modality of word presentation (left).

From Graf et al. . Copyright 1985 by the American Psychological Association. Reprinted with permission
Figure 16. Figure 16.

A tentative memory taxonomy. Declarative memory includes what can be declared or brought to mind, as a proposition or an image. It includes both episodic and semantic memory and the related terms, working and reference memory. Procedural memory includes motor skills, cognitive skills, and simple classical conditioning, as well as habituation, sensitization, various perceptual aftereffects, and other instances where the facility for engaging specific cognitive operations is improved by experience.

Figure 17. Figure 17.

Failure of several types of cortical insult to produce major functional disruption. These results were difficult to reconcile with electrical field theory or any hypothesis of cerebral organization based on horizontal intracortical conduction. A: multiple subpial knife cuts through the depth of the gray matter in sensorimotor cortex of monkey. B: similar knife cuts in visual cortex of cat. C: lateral and dorsal X‐ray views of tantalum wire insertions in visual cortex of cat. D: lateral X‐ray and dorsal surface views of mica plate insertions in visual cortex of cat.

From Sperry
Figure 18. Figure 18.

Ground plan of Lashley's Maze III, used extensively in his efforts to localize the engram. S, starting compartment; F, food compartment. Rats were given 5 trials per day until 10 consecutive errorless trials were recorded. Normal animals required 19 trials and 47 errors to learn the maze and 40 days later relearned it in 2 trials and 7 errors.

From Lashley
Figure 19. Figure 19.

Relationship between extent of cerebral lesion and errors in learning or relearning Lashley's Maze III. A: original learning (n = 37). Ordinate indicates the percentage of cortex removed for each animal; abscissa indicates the number of errors made during learning. B: relearning of the same maze task in rats with lesions made ∼2 wk after original learning (n = 59). Ordinate indicates the percentage of cortex removed; abscissa indicates the number of errors made during the postoperative retention test.

From Lashley
Figure 20. Figure 20.

Striking localization of function in the monkey. Monkeys with bilateral lesions of the middle third of the sulcus principalis (B) were unable to relearn the delayed‐alternation task, whereas lesions of the anterior (A) or posterior (C) thirds of the sulcus principalis had little effect. Three cross sections through different levels of the lesions are also shown for each brain. Blackened areas represent the extent of sulcus principalis damage; stippled areas indicate ineffective periarcuate and inferior parietal lesions. A.S., arcuate sulcus; C.S., central sulcus; I.P.S., inferior parietal sulcus; L.F., lateral fissure; L.S., lunate sulcus; P.S., sulcus principalis; S.T.S., superior temporal sulcus.

From Butters and Pandya . Copyright 1969 by the American Association for the Advancement of Science
Figure 21. Figure 21.

Marked localization of language functions in the peri‐sylvian region of the left hemisphere. Six language‐related functions were tested during neurosurgery for epilepsy in a 30‐yr‐old female, bilingual in English and Greek: naming of pictured objects in English (N) and Greek (G), reading of simple sentences (R), verbal memory across a short distraction‐filled interval (VI, VS, or VO), mimicry of single and sequential orofacial movements (M), and phoneme identification (P). Each site stimulated is represented by a rectangle; symbols within rectangles indicate that consistent errors of a particular type were made during electrical stimulation of that site. VI, memory with stimulation at the time of registration of information; VS, memory with stimulation during the distraction interval; VO, memory with stimulation at the time of retrieval; A, site of speech arrest; F, sites of evoked face movement and sensation. Frequently only one of the tested language functions was disrupted at any site. Naming in English and Greek could be separately disrupted.

From Ojemann
Figure 22. Figure 22.

Columnlike organization of interdigitating projections to frontal lobe in monkeys. Upper right: tritiated amino acids (H3–AA) were injected into sulcus principalis (PS) of the left hemisphere to label callosal projections to the PS in the right hemisphere. Horseradish peroxidase (HRP) pellets were implanted in the posterior bank of the intraparietal sulcus (IPS) in the right hemisphere to label projections to the right PS. In this way, convergent projections to PS, located in the rectangle, were labeled in the same animal. Left: composite of 2 coronal sections through the convergence zone in the sulcus principalis of the right hemisphere. Labeled termination zones for callosal fibers ( and ) are indicated by coarse stipples; termination zones for the parietofrontal projection ( and ) are indicated by fine stipples. Calibration bar, 0.5 mm. Although the organization of the 2 projections is irregular and sometimes overlapping, the 2 inputs are distributed in approximately alternating columns that extend across all 6 cortical layers.

From Goldman‐Rakic and Schwartz . Copyright 1982 by the American Association for the Advancement of Science
Figure 23. Figure 23.

Functional parcellation of cortex beyond the macrocolumn. Diagram proposes a modular organization of macaque striate cortex. Each ocular dominance column (L and R) contains cells sensitive to all orientations and is interpenetrated as well by cells that are sensitive to color but not orientation. Layer 4C, the site of termination of afferents from the lateral geniculate, is also insensitive to orientation.

From Livingstone and Hubel
Figure 24. Figure 24.

Diagram of the proposed neural circuit mediating a short‐latency (8‐ms) acoustic startle response in the rat. Arrows indicate synapses at points along the circuit. Habituation of the reflex appears to depend on changes in synapses formed by projections from ventral cochlear nucleus (VCN), ventral nucleus of the lateral lemniscus (VLL), or both. DLL, dorsal nucleus of the lateral lemniscus; CNIC, central nucleus of the inferior colliculus; DCN, dorsal cochlear nucleus; LM, medial lemniscus; MLF, medial longitudinal fasciculus; RGI, nucleus reticularis gigantocellularis; SO, superior olive; VAS, ventral acoustic stria; RPC, nucleus reticularis pontis caudalis. Labels to right show millimeters posterior to lambda.

From Davis et al.
Figure 25. Figure 25.

Diagram of pathways for visually conditioned heart‐rate change in the pigeon. Upper panel summarizes the visual pathways that transmit conditioned‐stimulus information (whole‐field illumination). Each of the 3 ascending pathways (1 to the thalamus and 2 to the tectum) is capable of transmitting effective conditioned‐stimulus information, but interruption of all 3 in combination prevents acquisition of the conditioned response. Brackets indicate equivalent mammalian structures. Middle panel describes the route by which the telencephalic targets of the conditioned‐stimulus pathway ultimately access the portion of the avian amygdaloid homologue that is considered the start of the descending pathway mediating expression of the conditioned response. Lower panel illustrates this descending (conditioned‐response) pathway. AMD, nucleus archistriatum mediale, pars dorsalis; HOM, tractus occipitomesencephalicus, pars hypothalami; HV, hyperstriatum ventrale; LGNe, dorsal lateral geniculate nucleus; MFB, medial forebrain bundle; NCM neostriatum caudale, pars mediale; NIM, neostriatum intermedium, pars mediale.

From Cohen
Figure 26. Figure 26.

Essential involvement of deep cerebellar nuclei in the classically conditioned eye‐blink response. A: sites where unit recordings did (filled circles) or did not (open circles) respond in relation to the amplitude and time course of the learned response. Large numbers above each section represent millimeters anterior to lambda; small numbers above each section represent millimeters lateral to midline. Small numbers to the side represent millimeters below bone at lambda. B; sites where stimulation did (filled circles) or did not (open circles) elicit eye‐blink responses. C: lesion of the dentate and interpositus nuclei that abolished the learned eye‐blink response to a tone without affecting the unconditioned eye‐blink response to an airpuff. D: composite of 3 lesions, shown in black, that were not effective in abolishing the learned response. ANS, ansiform lobule (crus I and crus II); ANT, anterior lobule; FL, flocculus; D, dentate nucleus; DCN, dorsal cochlear nucleus; F, fastigial nucleus; I, interpositus nucleus; IC, inferior colliculus; IO inferior olive; lob a, lobulus A (nodulus); PF, paraflocculus; VN, vestibular nuclei; cd, dorsal crus; cv, ventral crus; gvii, genu of the facial nerve; icp, inferior cerebellar penduncle; vii, facial nucleus; VCN, ventral cochlear nucleus; viii n, cranial nerve VIII.

From McCormick and Thompson . Copyright 1984 by the American Association for the Advancement of Science
Figure 27. Figure 27.

Loss of the nictitating membrane (NM) conditioned eyelid response (CR) in the rabbit after a lesion of the left dorsolateral part of the interpositus nucleus of the cerebellum. Performance of the left eye was good on the last day of paired conditioned stimulus‐unconditioned stimulus training (LP) before the lesion. L1‐L4, 4 days of training on the left eye after the lesion showing that the CR was abolished and not relearned; R1‐R4, 4 days of training on the right eye after the lesion showing initial savings (R1) and further learning; L5, final day of training on the left eye without improvement. Each data point shows the average score for 30 trials.

From Lavond et al.
Figure 28. Figure 28.

Lateral view of the monkey brain showing one route for the cortical processing of visual information from striate cortex (OC) to inferotemporal cortex (TE). Area TE, like other higher‐order cortical sensory areas, projects to amygdala (amyg) and to hippocampus (hippo) via hippocampal gyrus and perirhinal cortex. The fact that medial temporal lobe lesions, which include hippocampus and amygdala, cause amnesia but nevertheless spare many premorbid memories suggests that the spared memories are stored upstream from the lesion, i.e., in neocortex.

From Mishkin
Figure 29. Figure 29.

Diagram of the vocal control system in songbirds, parts of which show seasonal fluctuations in size corresponding to fluctuations in singing. Arrows indicate anterograde connections between nuclei. Neural signals for song originate in nucleus interfacialis (NIF) and end at the vocal organ, the syrinx, via nucleus hyperstriatum ventrale pars caudale (HVc), nucleus robustus archistriatalis (RA), dorsomedial nucleus of nucleus intercollicularis (DM), and nucleus hypoglossus pars tracheosyringealis (nXIIts), in that order. Other nuclei [magnocellular nucleus of the anterior neostriatum (MAN), area X (X), and nucleus uva (UVA)] are inactive during vocalization. Hatched areas indicate known projection zones of the telencephalic auditory area (field L).

From Konishi
Figure 30. Figure 30.

Summary maps from Penfield's series of patients showing where in each hemisphere experiential responses were produced by electrical stimulation. Top: lateral view. Middle: dorsal view. Frontal and parietal opercula have been removed to expose the plenum temporale. Bottom: ventral views. Experiential responses were obtained during 40 operations on 40 different patients out of the entire series of 1,132 patients. Experiential responses were obtained only in the temporal lobes in 7.7% of the 520 patients in which the temporal lobe was stimulated.

From Penfield and Perot
Figure 31. Figure 31.

Temporal lobe structures from which experiential responses were elicited by electrical stimulation with and without afterdischarge. Eighty‐eight experiential responses were obtained from 35 patients. Medial temporal lobe structures were involved, often together with neocortical structures, in 82 responses. Experiential phenomena usually required the participation of limbic structures.

From Gloor et al.
Figure 32. Figure 32.

A: representation of the course and primary branchings of the dorsal tegmental bundle (DTB), which originates in the catecholaminergic cell bodies of the locus coeruleus (LC) and widely innervates the forebrain. C, cingulum; CC, corpus callosum; F, fornix; FS, fornix superior; HC, hippocampus; HR, hippocampal rudiment; MFB, medial forebrain bundle; ON, olfactory nuclei; ST, stria terminalis. B: later it was appreciated that locus coeruleus neurons reach neocortex by a trajectory that passes through the frontal lobe and then caudally within neocortex through the full longitudinal extent of each hemisphere. M, medial axons innervating medial cortex; L, lateral axons innervating lateral cortex.

A from Lindvall and Björklund . B from Morrison et al. . Copyright 1979 by the American Association for the Advancement of Science
Figure 33. Figure 33.

Top left: effect of posttraining epinephrine on retention. Rats were trained on a 1‐trial passive avoidance task with a weak footshock. A: the most effective dose (0.1 mg/kg, given subcutaneously) significantly facilitated retention performance. B: as the injection of the best dose was delayed after training, its effect on memory decreased. Top right: effect of epinephrine on memory is influenced by the motivational conditions of training. Rats were trained using either a weak or strong footshock (FS) and given epinephrine immediately after training. Same dose that facilitated retention in the low‐footshock condition was disruptive in the high‐footshock condition. Bottom: epinephrine facilitated retention of control animals (ST‐sham) but had no effect on animals with lesions of stria terminalis (ST‐lesioned). Black areas (left) show step‐through latency of untrained animals. Numbers in parentheses show the number of animals in each group.

Top from Gold and McGaugh . Bottom from McGaugh . Copyright 1983 by the American Psychological Association. Reprinted by permission
Figure 34. Figure 34.

Top left: pathological findings in a representative case of Wernicke‐Korsakoff syndrome. Diencephalic localization of the lesions is shown in 3 coronal sections (from left to right) at the levels of the mammillary bodies, midthalamus, and pulvinar. Black areas show the extent of lesion. Bottom left: performance of 4 control monkeys (N) and 4 monkeys with lesions of the mediodorsal thalamic nucleus (MD) on the delayed nonmatching‐to‐sample task. Control monkeys required a mean of 140 trials to learn the task initially with a delay of 8 s, and the MD group required 315 trials. First point on the curve is the average final score during learning. Testing was then carried out at longer delays up to 10 min. Right, A: coronal sections through the thalamus showing the smallest (black areas) and the largest (hatched areas) extent of damage in the monkeys with MD lesions. Right, B: extent of fornix damage (hatched area) in 1 operated control animal. The extent of damage to MD averaged 38%. Adjacent thalamic nuclei were not consistently damaged. Cd, caudate nucleus; CM and CM‐Pf, centromedian nucleus; Hb, habenula; LD, lateral dorsal nucleus; LP, lateral posterior nucleus; MD, mediodorsal nucleus; VLc and VLps, ventral lateral nucleus; VPLc and VPLo, ventral posterolateral nucleus; VPM, ventral posteromedial nucleus.

Top left from Victor et al. ; bottom left and right from Zola‐Morgan and Squire
Figure 35. Figure 35.

Performance on 4 different tasks sensitive to human amnesia by normal monkeys (N) and monkeys with bilateral medial temporal lesions (H‐A) that included hippocampus, amygdala, and overlying cortex.

From Zola‐Morgan and Squire
Figure 36. Figure 36.

Combined data comparing the performance of normal monkeys (N), monkeys with hippocampal lesions (H), and monkeys with conjoint hippocampal‐amygdala lesions (HA) on the delayednonmatching‐to‐sample task.

Data from Mishkin , Mahut et al. , and Squire and Zola‐Morgan
Figure 37. Figure 37.

Different kinds of amnesic patients perform similarly on many tests of new learning ability. Here, 4 kinds of amnesic patients and matched control subjects (healthy subjects, alcoholics, or depressed psychiatric patients) were presented 10 pairs of unrelated words (e.g., army‐table) and then asked to recall the second word when given the first word of each pair. Recall was attempted after each of 3 successive presentations of the word pairs. Case NA became amnesic for verbal material in 1960 as the result of a penetrating injury from a miniature fencing foil that damaged the left dorsal thalamic region. Data are also shown for 8 patients with Korsakoff's syndrome, 8 psychiatric patients tested 1 h after the fourth or fifth treatment in a series of prescribed bilateral electroconvulsive therapy (ECT), and 4 patients who became amnesic as the result of an anoxic or ischemic episode.

Figure 38. Figure 38.

A: pattern of anterograde amnesia (A.A.) and retrograde amnesia (R.A.) in a severe case of head trauma, as determined by 3 clinical interviews after the trauma. Retrograde amnesia was temporally limited, with recent memory more affected than remote memory. B: temporally limited retrograde amnesia after electroconvulsive treatment, as determined by formal testing methods in mice and humans. Memory is considered to change for a long time after initial learning such that some material becomes unavailable (forgetting), while what remains becomes more resistant to disruption (consolidation).

A from Barbizet ; B from Squire
Figure 39. Figure 39.

Close connection between the medial temporal region and putative memory storage loci in the rest of cortex. Diagrams summarize cortical afferent and efferent connections of the rhesus monkey parahippocampal gyrus on lateral (inverted) and medial views of the cerebral hemisphere. Projections from widespread cortical areas converge on area 28 (entorhinal cortex), and most of these pathways are reciprocated by efferent projections.

From Van Hoesen
Figure 40. Figure 40.

Extensive remote‐memory impairment in patients with Korsakoff's syndrome in Boston (left) and San Diego (right), as measured by the same test of famous faces. Impairment is more severe for faces that came into the news in the most recent decade or two, presumably because anterograde amnesia was either already present or was gradually developing during this period. Impairment for more remote periods probably reflects true retrograde amnesia, i.e., loss of material that had been successfully learned before the onset of the syndrome. The higher level of performance in the San Diego population may reflect the easier method of cueing used for this group.

Left from Albert et al. ; right from Cohen and Squire
Figure 41. Figure 41.

Left: lateral view of the monkey brain. Drawing below photograph shows cytoarchitectonic areas according to von Bonin and Bailey . Vertical line through the frontal lobe shows the level of the coronal section to the right. as, Arcuate sulcus; cs, central sulcus; las, lateral sulcus; mos, medial orbital sulcus; ps, sulcus principalis. Right: coronal section illustrating the location of the lesions most commonly used to study frontal lobe function in the monkey. Numbers refer to cytoarchitectonic areas following nomenclature by Walker .

Left courtesy of D. G. Amaral
Figure 42. Figure 42.

Task‐specific impairments in short‐term or working memory caused by unilateral electrical stimulation of frontal or temporal neocortex. Horizontal lines indicate periods of stimulation. Top: performance on delayed response, with a cue presentation of 2 s and a delay of 8 s. Stimulation with 2‐s trains of 5.5‐ to 6.0‐mA current was applied to the posterior segment of inferotemporal cortex (temporal) or to dorsolateral frontal cortex (frontal) so that the electrodes straddled the sulcus principalis. Bottom: performance on delayed matching to sample, with a sample presentation of 2 s and a delay of 3 s. Vertical lines below time scale indicate the boundaries between sample, delay, match, and intertrial interval (ITI) portions of testing. Stimulation with 2‐s trains of 3.5‐ to 5.5‐ mA current was applied to the middle third of the temporal cortex (temporal) or to dorsolateral frontal cortex (frontal) so that the electrodes straddled the sulcus principalis.

Adapted from Stamm and Rosen and Kovner and Stamm
Figure 43. Figure 43.

Diagrams based on surgeon's drawings at the time of operation showing (in black) the estimated lateral extent of cortical excision in 7 representative cases of unilateral frontal lobectomy carried out for relief of focal epilepsy. Dots indicate points where electrical stimulation of the exposed cortex interfered with speech.

From Milner
Figure 44. Figure 44.

Impairment after unilateral frontal lobe lesions on a delayed‐comparison task. Two stimuli were presented 60 s apart, and subjects were asked to judge whether the second stimulus was the same as or different from the first. This task requires subjects not only to remember recent events but to suppress their memory for older similar occurrences so that judgments can be made about the most recent ones. Frontal patients performed well at nonsense figures, the only stimuli that were unique and did not repeat during testing.

From Milner . Reproduced with permission of McGraw‐Hill


Figure 1.

Diagram of a synapse onto a dendritic spine showing measures of synaptic morphology that have been used to study experience‐dependent structural alterations at synapses. Experience can also increase the number of synapses, presumably either by forming them outright or by selectively preserving some synapses from a population that is continuously being replaced.

From Chang and Greenough


Figure 2.

Morphological plasticity of synapses dependent on behavioral experience (top) or longterm potentiation (LTP) in hippocampus (bottom). Top: densities of synapses and neuronal nuclei were determined in upper occipital cortex (layers I‐IV), and these values were used to derive an estimate of the number of synapses per neuron. Rats were reared from 23 to 55 days of age in a complex environment (EC), in pairs in social cages (SC), or in individual cages (IC). Enriched rearing conditions resulted in an increased number of synapses per neuron. Neuronal density was decreased in EC animals because of a greater volume of neuronal somata, neuronal processes, and glia. Bottom: brief bursts of high‐frequency stimulation (100 Hz for 1 s or 200 Hz for 0.5 s) produced LTP of the Schaffer collateral‐CA1 system in rat. In the CA1 zone, LTP increased the number of synapses on the dendritic shafts (A) and the number of sessile spine synapses (B). Density of the much more common spine synapse was not affected.

From Greenough


Figure 3.

Three events in the development of specific connections in the vertebrate nervous system: cell death, axon collateral elimination, and synapse elimination. It is estimated that 50% of the nerve cells that are initially formed die before postnatal life. Process elimination by the surviving neurons involves both the removal of whole pathways and the elimination of functional synapses within remaining pathways. In this way, specific connections and networks are sculpted out of the initially formed nervous system.

From Cowan and O'Leary


Figure 4.

Pattern of arborization of a single geniculocortical afferent in the visual cortex of a 17‐day‐old kitten (left) and an adult cat (right). Prior to the segregation of cortical inputs into alternating left‐eye and right‐eye columns, the aborization of individual afferents extends uniformly over a disk‐shaped area >2 mm in diameter. This area is destined to be segregated into at least 4 columns. In the adult, after column formation is complete, individual afferents do not aborize uniformly. The arborization is divided into a number of clumps separated by gaps whose dimensions correspond to the size of individual ocular dominance columns. The gaps are filled with afferents serving the other eye.

From LeVay and Stryker


Figure 5.

Top left: ocular‐dominance distribution of 223 cells recorded from striate cortex of normal adult cats. Cells in groups 1 and 7 could be driven by only one eye. In groups 2, 3, 5, and 6, cells were driven better by one eye than the other. In group 4, cells were driven about equally by each eye. Bottom: ocular‐dominance distribution of 34 cells recorded from the left and right striate cortex of a cat without visual experience in the right eye from 9 wk to 6 mo of age. Majority of cells responded only to visual stimulation from the experienced eye. Top right: ocular‐dominance distribution of 126 cells recorded from cats without visual experience in either eye from ∼1 wk to ∼3 mo of age. Thirty‐seven cells did not respond to visual stimulation. In contrast to the effects of unilateral eye closure, after bilateral eye closure both eyes could drive cortical cells.

Adapted from Wiesel and Hubel


Figure 6.

Summary of cortical visual areas and their known connections. There are 2 major routes from striate cortex (V1): one follows a ventral route into the temporal lobe via area V4 and the other follows a dorsal route into the parietal lobe via MT. Filled arrowheads indicate “forward” projections; arrowheads indicate “backward” projections; lines with filled arrowheads at both ends indicate “intermediate” projections; d indicates that the projection is limited to the dorsal portion of the area; m indicates that it is limited to the medial portion. Other potential pathways into the parietal lobe include those carrying input from the peripheral visual field (dotted lines).

From Ungerleider and Desimone


Figure 7.

Recognition performance on the delayed nonmatching‐to‐sample test. Left: monkeys see an object and then 10 s later must choose the novel, unfamiliar object. Different objects are used on every trial. Right: performance by groups with bilateral lesions of posterior temporal cortex (TEO) or anterior temporal cortex (TE) and a group of unoperated controls (N). Numbers to the left of the curves are average numbers of trials needed after surgery to relearn the basic task, which involved remembering a single object for 10 s. First point on the curve is the average final score in this condition. Animals were subsequently tested in the same task with delay gradually increased from 10 s to 120 s.

Adapted from Mishkin


Figure 8.

A chess‐specific memory skill. Left: board position after the 25th move of Game 6 of the 1984 World Chess Championship in Moscow between A. Karpov (black) and G. Kasparov (white). Right: a random arrangement of the same 19 pieces. After briefly viewing the board of a real game, master players can reconstruct the board from memory much better than weaker players. With a randomly arranged board, experts and beginners perform the same.

See Chase and Simon for details


Figure 9.

Acquisition of a memory skill. In 20 mo involving ∼190 h of practice (1 h/day, 3–5 days/wk), a college student increased his digit span from 7 to 79 digits. Random digits were read to him at the rate of 1/s. If a sequence was recalled correctly, 1 digit was added to the next sequence.

From Ericsson et al. . Copyright 1980 by the American Association for the Advancement of Science


Figure 10.

Extended digit span. Five amnesic patients (including patient HM) and 20 control subjects were read a sequence of 5 digits. If the sequence was repeated back correctly, 1 digit was added to the next sequence; if not, the same sequence was given until it was repeated correctly. Amnesic patients had a normal digit span but required an abnormal number of trials to learn supraspan strings of digits. No amnesic patient recalled more than 12 digits within the testing limit of 25 trials.

From Drachman and Arbit . Copyright 1966, American Medical Association


Figure 11.

Serial‐position curves for 6 amnesic patients and 6 control subjects. Subjects were read 10‐word lists and then asked to recall them in any order. Percentage of items recalled is plotted as a function of their position in the list. Amnesic patients show the normal recency effect but an impaired primacy effect.

From Baddeley and Warrington


Figure 12.

Serial‐position curves for normal rats and rats with hippocampal lesions. Rats first visited 8 arms of a radial maze in a fixed sequence; 20 s (no delay) or 30 min (delay) later they were given a choice test involving arms 1 vs. 2, 4 vs. 5, or 7 vs. 8. They were rewarded for entering the arm that they had visited earlier. A: performance of normal animals showing both a primacy and recency effect in the no‐delay condition. B: performance of normal and operated animals in the no‐delay condition. C: performance of operated animals in the no‐delay and delay conditions.

From Kesner and Novak . Copyright 1982 by the American Association for the Advancement of Science


Figure 13.

Acquisition and retention of a mirror‐reading skill despite amnesia for the learning experience. A: patients prescribed bilateral (BIL) or right unilateral (RUL) electroconvulsive therapy and depressed patients (DEP) not receiving electroconvulsive therapy practiced mirror reading during 3 sessions (50 trials/session). For the patients receiving electroconvulsive therapy, 1 treatment intervened between the first 2 sessions, and an average of 7 treatments intervened between the second and third sessions. B: at the beginning of the third session, subjects were tested for their recollection of the previous testing sessions (9‐point interview) and for their memory of the words they had read (recognition test, chance = 50%).

From Squire et al. . Copyright 1984, Pergamon Press


Figure 14.

Intact priming in amnesia. Amnesic patients and control subjects saw common words and then were asked to recall the words (free recall) or were cued with the first 3 letters of the words and asked to recall them (cued recall). Amnesic patients were impaired in these 2 conditions but performed normally when they were given the first 3 letters of words and instructed simply to form the first word that came to mind (completion). Base‐line guessing rates in the word completion condition were 9%.

From Graf et al. . Copyright 1984 by the American Psychological Association. Reprinted by permission


Figure 15.

Diminution of priming effects across modality. Amnesic patients (AMN), alcoholic control subjects (ALC), and medical inpatients (INPT) read or heard words and then were cued visually with the first 3 letters of these words and asked to form the first words that came to mind. Priming was equivalent across groups and was higher when the study words and the test cues were in the same modality (right). (Hatching shows base‐line word‐completion performance when the words were not presented for study.) Amnesic patients were markedly impaired at recalling words, and recall was unaffected by the modality of word presentation (left).

From Graf et al. . Copyright 1985 by the American Psychological Association. Reprinted with permission


Figure 16.

A tentative memory taxonomy. Declarative memory includes what can be declared or brought to mind, as a proposition or an image. It includes both episodic and semantic memory and the related terms, working and reference memory. Procedural memory includes motor skills, cognitive skills, and simple classical conditioning, as well as habituation, sensitization, various perceptual aftereffects, and other instances where the facility for engaging specific cognitive operations is improved by experience.



Figure 17.

Failure of several types of cortical insult to produce major functional disruption. These results were difficult to reconcile with electrical field theory or any hypothesis of cerebral organization based on horizontal intracortical conduction. A: multiple subpial knife cuts through the depth of the gray matter in sensorimotor cortex of monkey. B: similar knife cuts in visual cortex of cat. C: lateral and dorsal X‐ray views of tantalum wire insertions in visual cortex of cat. D: lateral X‐ray and dorsal surface views of mica plate insertions in visual cortex of cat.

From Sperry


Figure 18.

Ground plan of Lashley's Maze III, used extensively in his efforts to localize the engram. S, starting compartment; F, food compartment. Rats were given 5 trials per day until 10 consecutive errorless trials were recorded. Normal animals required 19 trials and 47 errors to learn the maze and 40 days later relearned it in 2 trials and 7 errors.

From Lashley


Figure 19.

Relationship between extent of cerebral lesion and errors in learning or relearning Lashley's Maze III. A: original learning (n = 37). Ordinate indicates the percentage of cortex removed for each animal; abscissa indicates the number of errors made during learning. B: relearning of the same maze task in rats with lesions made ∼2 wk after original learning (n = 59). Ordinate indicates the percentage of cortex removed; abscissa indicates the number of errors made during the postoperative retention test.

From Lashley


Figure 20.

Striking localization of function in the monkey. Monkeys with bilateral lesions of the middle third of the sulcus principalis (B) were unable to relearn the delayed‐alternation task, whereas lesions of the anterior (A) or posterior (C) thirds of the sulcus principalis had little effect. Three cross sections through different levels of the lesions are also shown for each brain. Blackened areas represent the extent of sulcus principalis damage; stippled areas indicate ineffective periarcuate and inferior parietal lesions. A.S., arcuate sulcus; C.S., central sulcus; I.P.S., inferior parietal sulcus; L.F., lateral fissure; L.S., lunate sulcus; P.S., sulcus principalis; S.T.S., superior temporal sulcus.

From Butters and Pandya . Copyright 1969 by the American Association for the Advancement of Science


Figure 21.

Marked localization of language functions in the peri‐sylvian region of the left hemisphere. Six language‐related functions were tested during neurosurgery for epilepsy in a 30‐yr‐old female, bilingual in English and Greek: naming of pictured objects in English (N) and Greek (G), reading of simple sentences (R), verbal memory across a short distraction‐filled interval (VI, VS, or VO), mimicry of single and sequential orofacial movements (M), and phoneme identification (P). Each site stimulated is represented by a rectangle; symbols within rectangles indicate that consistent errors of a particular type were made during electrical stimulation of that site. VI, memory with stimulation at the time of registration of information; VS, memory with stimulation during the distraction interval; VO, memory with stimulation at the time of retrieval; A, site of speech arrest; F, sites of evoked face movement and sensation. Frequently only one of the tested language functions was disrupted at any site. Naming in English and Greek could be separately disrupted.

From Ojemann


Figure 22.

Columnlike organization of interdigitating projections to frontal lobe in monkeys. Upper right: tritiated amino acids (H3–AA) were injected into sulcus principalis (PS) of the left hemisphere to label callosal projections to the PS in the right hemisphere. Horseradish peroxidase (HRP) pellets were implanted in the posterior bank of the intraparietal sulcus (IPS) in the right hemisphere to label projections to the right PS. In this way, convergent projections to PS, located in the rectangle, were labeled in the same animal. Left: composite of 2 coronal sections through the convergence zone in the sulcus principalis of the right hemisphere. Labeled termination zones for callosal fibers ( and ) are indicated by coarse stipples; termination zones for the parietofrontal projection ( and ) are indicated by fine stipples. Calibration bar, 0.5 mm. Although the organization of the 2 projections is irregular and sometimes overlapping, the 2 inputs are distributed in approximately alternating columns that extend across all 6 cortical layers.

From Goldman‐Rakic and Schwartz . Copyright 1982 by the American Association for the Advancement of Science


Figure 23.

Functional parcellation of cortex beyond the macrocolumn. Diagram proposes a modular organization of macaque striate cortex. Each ocular dominance column (L and R) contains cells sensitive to all orientations and is interpenetrated as well by cells that are sensitive to color but not orientation. Layer 4C, the site of termination of afferents from the lateral geniculate, is also insensitive to orientation.

From Livingstone and Hubel


Figure 24.

Diagram of the proposed neural circuit mediating a short‐latency (8‐ms) acoustic startle response in the rat. Arrows indicate synapses at points along the circuit. Habituation of the reflex appears to depend on changes in synapses formed by projections from ventral cochlear nucleus (VCN), ventral nucleus of the lateral lemniscus (VLL), or both. DLL, dorsal nucleus of the lateral lemniscus; CNIC, central nucleus of the inferior colliculus; DCN, dorsal cochlear nucleus; LM, medial lemniscus; MLF, medial longitudinal fasciculus; RGI, nucleus reticularis gigantocellularis; SO, superior olive; VAS, ventral acoustic stria; RPC, nucleus reticularis pontis caudalis. Labels to right show millimeters posterior to lambda.

From Davis et al.


Figure 25.

Diagram of pathways for visually conditioned heart‐rate change in the pigeon. Upper panel summarizes the visual pathways that transmit conditioned‐stimulus information (whole‐field illumination). Each of the 3 ascending pathways (1 to the thalamus and 2 to the tectum) is capable of transmitting effective conditioned‐stimulus information, but interruption of all 3 in combination prevents acquisition of the conditioned response. Brackets indicate equivalent mammalian structures. Middle panel describes the route by which the telencephalic targets of the conditioned‐stimulus pathway ultimately access the portion of the avian amygdaloid homologue that is considered the start of the descending pathway mediating expression of the conditioned response. Lower panel illustrates this descending (conditioned‐response) pathway. AMD, nucleus archistriatum mediale, pars dorsalis; HOM, tractus occipitomesencephalicus, pars hypothalami; HV, hyperstriatum ventrale; LGNe, dorsal lateral geniculate nucleus; MFB, medial forebrain bundle; NCM neostriatum caudale, pars mediale; NIM, neostriatum intermedium, pars mediale.

From Cohen


Figure 26.

Essential involvement of deep cerebellar nuclei in the classically conditioned eye‐blink response. A: sites where unit recordings did (filled circles) or did not (open circles) respond in relation to the amplitude and time course of the learned response. Large numbers above each section represent millimeters anterior to lambda; small numbers above each section represent millimeters lateral to midline. Small numbers to the side represent millimeters below bone at lambda. B; sites where stimulation did (filled circles) or did not (open circles) elicit eye‐blink responses. C: lesion of the dentate and interpositus nuclei that abolished the learned eye‐blink response to a tone without affecting the unconditioned eye‐blink response to an airpuff. D: composite of 3 lesions, shown in black, that were not effective in abolishing the learned response. ANS, ansiform lobule (crus I and crus II); ANT, anterior lobule; FL, flocculus; D, dentate nucleus; DCN, dorsal cochlear nucleus; F, fastigial nucleus; I, interpositus nucleus; IC, inferior colliculus; IO inferior olive; lob a, lobulus A (nodulus); PF, paraflocculus; VN, vestibular nuclei; cd, dorsal crus; cv, ventral crus; gvii, genu of the facial nerve; icp, inferior cerebellar penduncle; vii, facial nucleus; VCN, ventral cochlear nucleus; viii n, cranial nerve VIII.

From McCormick and Thompson . Copyright 1984 by the American Association for the Advancement of Science


Figure 27.

Loss of the nictitating membrane (NM) conditioned eyelid response (CR) in the rabbit after a lesion of the left dorsolateral part of the interpositus nucleus of the cerebellum. Performance of the left eye was good on the last day of paired conditioned stimulus‐unconditioned stimulus training (LP) before the lesion. L1‐L4, 4 days of training on the left eye after the lesion showing that the CR was abolished and not relearned; R1‐R4, 4 days of training on the right eye after the lesion showing initial savings (R1) and further learning; L5, final day of training on the left eye without improvement. Each data point shows the average score for 30 trials.

From Lavond et al.


Figure 28.

Lateral view of the monkey brain showing one route for the cortical processing of visual information from striate cortex (OC) to inferotemporal cortex (TE). Area TE, like other higher‐order cortical sensory areas, projects to amygdala (amyg) and to hippocampus (hippo) via hippocampal gyrus and perirhinal cortex. The fact that medial temporal lobe lesions, which include hippocampus and amygdala, cause amnesia but nevertheless spare many premorbid memories suggests that the spared memories are stored upstream from the lesion, i.e., in neocortex.

From Mishkin


Figure 29.

Diagram of the vocal control system in songbirds, parts of which show seasonal fluctuations in size corresponding to fluctuations in singing. Arrows indicate anterograde connections between nuclei. Neural signals for song originate in nucleus interfacialis (NIF) and end at the vocal organ, the syrinx, via nucleus hyperstriatum ventrale pars caudale (HVc), nucleus robustus archistriatalis (RA), dorsomedial nucleus of nucleus intercollicularis (DM), and nucleus hypoglossus pars tracheosyringealis (nXIIts), in that order. Other nuclei [magnocellular nucleus of the anterior neostriatum (MAN), area X (X), and nucleus uva (UVA)] are inactive during vocalization. Hatched areas indicate known projection zones of the telencephalic auditory area (field L).

From Konishi


Figure 30.

Summary maps from Penfield's series of patients showing where in each hemisphere experiential responses were produced by electrical stimulation. Top: lateral view. Middle: dorsal view. Frontal and parietal opercula have been removed to expose the plenum temporale. Bottom: ventral views. Experiential responses were obtained during 40 operations on 40 different patients out of the entire series of 1,132 patients. Experiential responses were obtained only in the temporal lobes in 7.7% of the 520 patients in which the temporal lobe was stimulated.

From Penfield and Perot


Figure 31.

Temporal lobe structures from which experiential responses were elicited by electrical stimulation with and without afterdischarge. Eighty‐eight experiential responses were obtained from 35 patients. Medial temporal lobe structures were involved, often together with neocortical structures, in 82 responses. Experiential phenomena usually required the participation of limbic structures.

From Gloor et al.


Figure 32.

A: representation of the course and primary branchings of the dorsal tegmental bundle (DTB), which originates in the catecholaminergic cell bodies of the locus coeruleus (LC) and widely innervates the forebrain. C, cingulum; CC, corpus callosum; F, fornix; FS, fornix superior; HC, hippocampus; HR, hippocampal rudiment; MFB, medial forebrain bundle; ON, olfactory nuclei; ST, stria terminalis. B: later it was appreciated that locus coeruleus neurons reach neocortex by a trajectory that passes through the frontal lobe and then caudally within neocortex through the full longitudinal extent of each hemisphere. M, medial axons innervating medial cortex; L, lateral axons innervating lateral cortex.

A from Lindvall and Björklund . B from Morrison et al. . Copyright 1979 by the American Association for the Advancement of Science


Figure 33.

Top left: effect of posttraining epinephrine on retention. Rats were trained on a 1‐trial passive avoidance task with a weak footshock. A: the most effective dose (0.1 mg/kg, given subcutaneously) significantly facilitated retention performance. B: as the injection of the best dose was delayed after training, its effect on memory decreased. Top right: effect of epinephrine on memory is influenced by the motivational conditions of training. Rats were trained using either a weak or strong footshock (FS) and given epinephrine immediately after training. Same dose that facilitated retention in the low‐footshock condition was disruptive in the high‐footshock condition. Bottom: epinephrine facilitated retention of control animals (ST‐sham) but had no effect on animals with lesions of stria terminalis (ST‐lesioned). Black areas (left) show step‐through latency of untrained animals. Numbers in parentheses show the number of animals in each group.

Top from Gold and McGaugh . Bottom from McGaugh . Copyright 1983 by the American Psychological Association. Reprinted by permission


Figure 34.

Top left: pathological findings in a representative case of Wernicke‐Korsakoff syndrome. Diencephalic localization of the lesions is shown in 3 coronal sections (from left to right) at the levels of the mammillary bodies, midthalamus, and pulvinar. Black areas show the extent of lesion. Bottom left: performance of 4 control monkeys (N) and 4 monkeys with lesions of the mediodorsal thalamic nucleus (MD) on the delayed nonmatching‐to‐sample task. Control monkeys required a mean of 140 trials to learn the task initially with a delay of 8 s, and the MD group required 315 trials. First point on the curve is the average final score during learning. Testing was then carried out at longer delays up to 10 min. Right, A: coronal sections through the thalamus showing the smallest (black areas) and the largest (hatched areas) extent of damage in the monkeys with MD lesions. Right, B: extent of fornix damage (hatched area) in 1 operated control animal. The extent of damage to MD averaged 38%. Adjacent thalamic nuclei were not consistently damaged. Cd, caudate nucleus; CM and CM‐Pf, centromedian nucleus; Hb, habenula; LD, lateral dorsal nucleus; LP, lateral posterior nucleus; MD, mediodorsal nucleus; VLc and VLps, ventral lateral nucleus; VPLc and VPLo, ventral posterolateral nucleus; VPM, ventral posteromedial nucleus.

Top left from Victor et al. ; bottom left and right from Zola‐Morgan and Squire


Figure 35.

Performance on 4 different tasks sensitive to human amnesia by normal monkeys (N) and monkeys with bilateral medial temporal lesions (H‐A) that included hippocampus, amygdala, and overlying cortex.

From Zola‐Morgan and Squire


Figure 36.

Combined data comparing the performance of normal monkeys (N), monkeys with hippocampal lesions (H), and monkeys with conjoint hippocampal‐amygdala lesions (HA) on the delayednonmatching‐to‐sample task.

Data from Mishkin , Mahut et al. , and Squire and Zola‐Morgan


Figure 37.

Different kinds of amnesic patients perform similarly on many tests of new learning ability. Here, 4 kinds of amnesic patients and matched control subjects (healthy subjects, alcoholics, or depressed psychiatric patients) were presented 10 pairs of unrelated words (e.g., army‐table) and then asked to recall the second word when given the first word of each pair. Recall was attempted after each of 3 successive presentations of the word pairs. Case NA became amnesic for verbal material in 1960 as the result of a penetrating injury from a miniature fencing foil that damaged the left dorsal thalamic region. Data are also shown for 8 patients with Korsakoff's syndrome, 8 psychiatric patients tested 1 h after the fourth or fifth treatment in a series of prescribed bilateral electroconvulsive therapy (ECT), and 4 patients who became amnesic as the result of an anoxic or ischemic episode.



Figure 38.

A: pattern of anterograde amnesia (A.A.) and retrograde amnesia (R.A.) in a severe case of head trauma, as determined by 3 clinical interviews after the trauma. Retrograde amnesia was temporally limited, with recent memory more affected than remote memory. B: temporally limited retrograde amnesia after electroconvulsive treatment, as determined by formal testing methods in mice and humans. Memory is considered to change for a long time after initial learning such that some material becomes unavailable (forgetting), while what remains becomes more resistant to disruption (consolidation).

A from Barbizet ; B from Squire


Figure 39.

Close connection between the medial temporal region and putative memory storage loci in the rest of cortex. Diagrams summarize cortical afferent and efferent connections of the rhesus monkey parahippocampal gyrus on lateral (inverted) and medial views of the cerebral hemisphere. Projections from widespread cortical areas converge on area 28 (entorhinal cortex), and most of these pathways are reciprocated by efferent projections.

From Van Hoesen


Figure 40.

Extensive remote‐memory impairment in patients with Korsakoff's syndrome in Boston (left) and San Diego (right), as measured by the same test of famous faces. Impairment is more severe for faces that came into the news in the most recent decade or two, presumably because anterograde amnesia was either already present or was gradually developing during this period. Impairment for more remote periods probably reflects true retrograde amnesia, i.e., loss of material that had been successfully learned before the onset of the syndrome. The higher level of performance in the San Diego population may reflect the easier method of cueing used for this group.

Left from Albert et al. ; right from Cohen and Squire


Figure 41.

Left: lateral view of the monkey brain. Drawing below photograph shows cytoarchitectonic areas according to von Bonin and Bailey . Vertical line through the frontal lobe shows the level of the coronal section to the right. as, Arcuate sulcus; cs, central sulcus; las, lateral sulcus; mos, medial orbital sulcus; ps, sulcus principalis. Right: coronal section illustrating the location of the lesions most commonly used to study frontal lobe function in the monkey. Numbers refer to cytoarchitectonic areas following nomenclature by Walker .

Left courtesy of D. G. Amaral


Figure 42.

Task‐specific impairments in short‐term or working memory caused by unilateral electrical stimulation of frontal or temporal neocortex. Horizontal lines indicate periods of stimulation. Top: performance on delayed response, with a cue presentation of 2 s and a delay of 8 s. Stimulation with 2‐s trains of 5.5‐ to 6.0‐mA current was applied to the posterior segment of inferotemporal cortex (temporal) or to dorsolateral frontal cortex (frontal) so that the electrodes straddled the sulcus principalis. Bottom: performance on delayed matching to sample, with a sample presentation of 2 s and a delay of 3 s. Vertical lines below time scale indicate the boundaries between sample, delay, match, and intertrial interval (ITI) portions of testing. Stimulation with 2‐s trains of 3.5‐ to 5.5‐ mA current was applied to the middle third of the temporal cortex (temporal) or to dorsolateral frontal cortex (frontal) so that the electrodes straddled the sulcus principalis.

Adapted from Stamm and Rosen and Kovner and Stamm


Figure 43.

Diagrams based on surgeon's drawings at the time of operation showing (in black) the estimated lateral extent of cortical excision in 7 representative cases of unilateral frontal lobectomy carried out for relief of focal epilepsy. Dots indicate points where electrical stimulation of the exposed cortex interfered with speech.

From Milner


Figure 44.

Impairment after unilateral frontal lobe lesions on a delayed‐comparison task. Two stimuli were presented 60 s apart, and subjects were asked to judge whether the second stimulus was the same as or different from the first. This task requires subjects not only to remember recent events but to suppress their memory for older similar occurrences so that judgments can be made about the most recent ones. Frontal patients performed well at nonsense figures, the only stimuli that were unique and did not repeat during testing.

From Milner . Reproduced with permission of McGraw‐Hill
References
 1. Aggleton, J. P., and M. Mishkin. Visual recognition impairment following medial thalamic lesions in monkeys. Neuropsychologia 21: 189–197, 1983.
 2. Aggleton, J. P., and M. Mishkin. Memory impairments following restricted medial thalamic lesions in monkeys. Exp. Brain Res. 52: 199–209, 1983.
 3. Aggleton, J. P., and M. Mishkin. Mammillary‐body lesions and visual recognition in the monkey. Exp. Brain Res. 58: 190–197, 1985.
 4. Agranoff, B. W., H. R. Burrell, L. A. Dokas, and A. D. Springer. Progress in biochemical approaches to learning and memory. In: Psychopharmacology: A Generation of Progress, edited by M. A. Lipton, A. DiMascio, and K. F. Killam. New York: Raven, 1978, p. 623–635.
 5. Aigner, T., S. Mitchell, J. Aggleton, M. De Long, R. Struble, G. Wenk, D. Price, and M. Mishkin. Recognition deficit in monkeys following neurotoxic lesions of the basal forebrain. Soc. Neurosci. Abstr. 10: 386, 1984.
 6. Albert, M. S., N. Butters, and J. Levin. Temporal gradients in the retrograde amnesia of patients with alcoholic Korsakoff's disease. Arch. Neurol. 36: 211–216, 1979.
 7. Albus, J. S. A theory of cerebellar function. Math. Biosci. 10: 26–61, 1971.
 8. Alexander, M. P., and M. Freedman. Amnesia after anterior communicating artery aneurysm rupture. Neurology 34: 752–757, 1984.
 9. Alkon, D. L. Calcium mediated reduction of ionic currents: a biophysical memory trace. Science Wash. DC 226: 1037–1045, 1984.
 10. Alkon, D. L., and J. Farley (editors). Primary Neural Substrates of Learning and Behavorial Change. New York: Cambridge Univ. Press, 1984.
 11. Allman, J. M. Evolution of the visual system in the early primates. Prog. Psychobiol. Physiol. Psychol. 7: 1–53, 1977.
 12. Amaral, D. G., and J. A. Foss. Locus coeruleus lesions and learning. Science Wash. DC 188: 377–378, 1975.
 13. Anderson, J. R. Language, Memory, and Thought. Hillsdale, NJ: Erlbaum, 1976.
 14. Anderson, J. R. Cognitive Psychology and Its Implications. San Francisco, CA: Freeman, 1980.
 15. Anlezark, G. M., T. J. Crow, and A. P. Greenway. Impaired learning and decreased cortical norepinephrine after bilateral locus coeruleus lesions. Science Wash. DC 181: 682–684, 1973.
 16. Arnsten, A. F. T., and D. S. Segal. Naloxone alters locomotion and interaction with environmental stimuli. Life Sci. 25: 1035–1042, 1979.
 17. Arnsten, A. F. T., D. S. Segal, H. J. Neville, S. A. Hillyard, D. S. Janowsky, L. L. Judd, and F. E. Bloom. Naloxone augments electrophysiological signs of selective attention in man. Nature Lond. 304: 725–727, 1983.
 18. Aston‐Jones, G., and F. E. Bloom. Norepinephrine‐containing locus coeruleus neurons in behaving rats exhibit pronounced responses to non‐noxious environmental stimuli. J. Neurosci. 1: 887–900, 1981.
 19. Atkinson, R. C., and R. M. Shiffrin. Human memory: a proposed system and its control processes. In: The Psychology of Learning and Motivation: Advances in Research and Theory, edited by K. W. Spence and J. T. Spence. New York: Academic, 1968, vol. 2, p. 89–195.
 20. Azmitia, E. C. The serotonin‐producing neurons of the midbrain median and the dorsal raphe nuclei. In: Handbook of Psychopharmacology. Chemical Pathways in the Brain, edited by L. L. Iversen, S. D. Iversen, and S. H. Snyder. New York: Plenum, 1978, vol. 9, p. 223–314.
 21. Bachevalier, J., and M. Mishkin. An early and a late developing system for learning and retention in infant monkeys. Behav. Neurosci. 98: 770–778, 1984.
 22. Baddeley, A. D. The concept of working memory: a view of its current state and probable future development. Cognition 10: 17–23, 1981.
 23. Baddeley, A. D. Implications of neuropsychological evidence for theories of normal memory. Philos. Trans. R. Soc. Lond. B Biol. Sci. 298: 59–72, 1982.
 24. Baddeley, A. D., and G. J. Hitch. Working memory. In: The Psychology of Learning and Motivation: Advances in Research and Theory, edited by G. H. Bower. New York: Academic, 1974, vol. 8, p. 47–90.
 25. Baddeley, A. D., and E. K. Warrington. Amnesia and the distinction between long‐ and short‐term memory. J. Verb. Learn. Verb. Behav. 9: 176–189, 1970.
 26. Bailey, C. H., and M. Chen. Morphological basis of long‐term habituation and sensitization in Aplysia. Science Wash. DC 220: 91–93, 1983.
 27. Bailey, P., G. von Bonin, and W. McCulloch. The Isocortex of the Chimpanzee. Urbana: Univ. of Illinois Press, 1950.
 28. Baldwin, M. Electrical stimulation of the medial temporal region. In: Electrical Studies on the Unanesthetized Brain, edited by E. R. Ramey and D. S. O'Doherty. New York: Hoeber, 1961, p. 159–176.
 29. Barbizet, J. Human Memory and its Pathology. San Francisco, CA: Freeman, 1970.
 30. Barbizet, J., J. D. Degos, F. Louarn, J. P. Nguyen, and J. L. Mas. Amnésie par lésion ischémique bi‐thalamique. Rev. Neurol. 137: 415–424, 1981.
 31. Barondes, S. H. Cerebral protein synthesis inhibitors block long‐term memory. Int. Rev. Neurobiol. 12: 177–205, 1970.
 32. Barondes, S. H. Protein‐synthesis dependent and protein‐synthesis independent memory storage processes. In: Short‐Term Memory, edited by D. Deutsch and J. A. Deutsch. New York: Academic, 1975, p. 379–390.
 33. Bartlett, F., and E. R. John. Equipotentiality quantified: the anatomical distribution of the engram. Science Wash. DC 181: 764–767, 1973.
 34. Bartus, R. T., R. L. Dean, B. Beer, and A. S. Lippa. The cholinergic hypothesis of geriatric memory dysfunction. Science Wash. DC 217: 408–417; 1982.
 35. Bateson, P. P. G. The neural basis of imprinting. In: The Biology of Learning, edited by P. Marler and H. Terrace. Berlin: Springer‐Verlag, 1984, p. 325–339. (Dahlem Konferenzen.)
 36. Bear, M. F., and J. D. Daniels. The plastic response to monocular deprivation persists in kitten visual cortex after chronic depletion of norepinephrine. J. Neurosci. 3: 407–416, 1983.
 37. Bennett, C., K. C. Liang, and J. L. McGaugh. Epinephrine alters the effect of amygdala stimulation on retention of avoidance tasks. Soc. Neurosci. Abstr. 8: 459, 1982.
 38. Benson, D. F., C. D. Marsden, and J. L. Meadows. The amnesic syndrome of posterior cerebral artery occlusion. Acta Neurol. Scand. 50: 133–145, 1974.
 39. Berger, T. W., and R. F. Thompson. Identification of pyramidal cells as the critical elements in hippocampal neuronal plasticity during learning. Proc. Natl. Acad. Sci. USA 75: 1572–1576, 1978.
 40. Bergson, H. Matter and Memory. London: Allen & Unwin, 1911.
 41. Black, P., and R. E. Myers. Brainstem mediation of visual perception in a higher primate. Trans. Am. Neurol. Assoc. 93: 191–193, 1968.
 42. Blakemore, C. Developmental factors in the formation of feature extracting neurons. In: The Neurosciences: Third Study Program, edited by F. O. Schmitt and F. G. Worden. Cambridge, MA: MIT Press, 1974, p. 105–113.
 43. Blakemore, C., and G. F. Cooper. Development of the brain depends on the visual environment. Nature Lond. 228: 477–478, 1970.
 44. Blakemore, C., and R. C. Van Sluyters. Reversal of the physiological effects of monocular deprivation in kittens: further evidence for a sensitive period. J. Physiol. Lond. 237: 195–216, 1974.
 45. Blanchard, D. C., and R. J. Blanchard. Innate and conditioned reactions to threat in rats with amygdaloid lesions. J. Comp. Physiol. Psychol. 81: 281–290, 1972.
 46. Bliss, T. V. P., and T. Lømo. Long‐lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J. Physiol. Lond. 232: 331–356, 1973.
 47. Blum, R. A. Effects of subtotal lesions of frontal granular cortex on delayed reaction in monkeys. Arch. Neurol. Psychiatry 67: 375–386, 1952.
 48. Brierley, J. B. Neuropathology of amnesic states. In: Amnesia, edited by C. W. M. Whitty and O. L. Zangwill. London: Butterworths, 1977, p. 199–223.
 49. Brion, S., and J. Mikol. Atteinte du noyau latéral dorsal du thalamus et syndrome de Korsakoff alcoolique. J. Neurol. Sci. 38: 249–261, 1978.
 50. Broca, P. P. Remarks on the seat of the faculty of articulate language, followed by an observation of aphemia. In: Some Papers on the Cerebral Cortex, translated by G. von Bonin. Springfield, IL: Thomas, 1960, p. 49–72.
 51. Brooks, D. N., and A. D. Baddeley. What can amnesic patients learn? Neuropsychologia 14: 111–122, 1976.
 52. Brown, R., and J. Kulik. Flashbulb memories. Cognition 5: 73–99, 1977.
 53. Bruner, J. S. Modalities of memory. In: The Pathology of Memory, edited by G. A. Talland and N. C. Waugh. New York: Academic, 1969, p. 253–259.
 54. Bullock, T. H. Reassessment of neural connectivity and its specification. In: Information Processing in the Nervous System, edited by H. M. Pinsker and W. D. Willis, Jr. New York: Raven, 1980, p. 199–220.
 55. Burnham, W. H. Retroactive amnesia: illustrative cases and a tentative explanation. Am. J. Psychol. 14: 382–396, 1903.
 56. Butler, C. R. A memory‐record for visual discrimination habits produced in both cerebral hemispheres of monkey when only one hemisphere has received direct visual information. Brain Res. 10: 152–167, 1968.
 57. Butters, N. Alcoholic Korsakoff's syndrome: an update. Semin. Neurol. 4: 226–244, 1984.
 58. Butters, N., and D. Pandya. Retention of delayed‐alternation: effect of selective lesions of sulcus principalis. Science Wash. DC 165: 1271–1273, 1969.
 59. Cermak, L. S. (editor). Human Memory and Amnesia. Hillsdale, NJ: Erlbaum, 1982.
 60. Cermak, L. S., N. Butters, and J. Moreines. Some analyses of the verbal encoding deficit of alcoholic Korsakoff patients. Brain Lang. 1: 141–150, 1974.
 61. Chang, T. J., and A. Gelperin. Rapid taste‐aversion learning by an isolated molluscan central nervous system. Proc. Natl. Acad. Sci. USA 77: 6204–6206, 1980.
 62. Chang, F. F., and W. T. Greenough. Lateralized effects of monocular training on dendritic branching in adult split‐brain rats. Brain Res. 232: 283–292, 1982.
 63. Chang, F. F., and W. T. Greenough. Transient and enduring morphological correlates of synaptic activity and efficacy change in the rat hippocampal slice. Brain Res. 309: 35–46, 1984.
 64. Changeux, J., and A. Danchin. Selective stabilisation of developing synapses as a mechanism for the specification of neuronal networks. Nature Lond. 246: 705–712, 1976.
 65. Chase, W. G., and H. A. Simon. Perception in chess. Cognit. Psychol. 4: 55–81, 1973.
 66. Cipolla‐Neto, J., G. Horn, and B. J. McCabe. Hemispheric asymmetry and imprinting: the effect of sequential lesions to the hyperstriatum ventrale. Exp. Brain Res. 48: 22–27, 1982.
 67. Cohen, D. H. Involvement of the avian amygdalar homologue (archistriatum posterior and mediale) in defensively conditioned heart rate change. J. Comp. Neurol. 160: 13–36, 1975.
 68. Cohen, D. H. The functional neuroanatomy of a conditioned response. In: Neural Mechanisms of Goal‐Directed Behavior and Learning, edited by R. F. Thompson, L. H. Hicks, and V. B. Shvyrkov. New York: Academic, 1980. p. 283–302.
 69. Cohen, D. H. Identification of vertebrate neurons modified during learning: analysis of sensory pathways. In: Primary Neural Substrates of Learning and Behavioral Change, edited by D. L. Alkon and J. Farley. New York: Cambridge Univ. Press, 1984, p. 129–154.
 70. Cohen, D. H. Some organizational principles of a vertebrate conditioning pathway: is memory a distributed property? In: Memory Systems of the Brain: Animal and Human Cognitive Processes, edited by N. Weinberger, J. McGaugh, and G. Lynch. New York: Guilford, 1985, p. 27–48.
 71. Cohen, D. H., and R. L. MacDonald. Involvement of the avian hypothalamus in defensively conditioned heart rate change. J. Comp. Neurol. 167: 465–480, 1976.
 72. Cohen, N. J. Neuropsychological Evidence for a Distinction Between Procedural and Declarative Knowledge in Human Memory and Amnesia. San Diego: Univ. of California Press, 1981. PhD thesis.
 73. Cohen, N. J. Preserved learning capacity in amnesia: evidence for multiple memory systems. In: Neuropsychology of Memory, edited by L. R. Squire and N. Butters. New York: Guilford, 1984, p. 83–103.
 74. Cohen, N. J., and L. R. Squire. Preserved learning and retention of pattern‐analyzing skill in amnesia: dissociation of knowing how and knowing that. Science Wash. DC 210: 207–209, 1980.
 75. Cohen, N. J., and L. R. Squire. Retrograde amnesia and remote memory impairment. Neuropsychologia 19: 337–356, 1981.
 76. Corkin, S. Lasting consequences of bilateral medial temporal lobectomy: clinical course and experimental findings in H. M. Semin. Neurol. 4: 249–259, 1984.
 77. Cowan, W. M. Neuronal death as a regulative mechanism in the control of cell number in the nervous system. In: Development and Aging in the Nervous System, edited by M. Rockstein and M. L. Sussman. New York: Academic, 1973, p. 19–41.
 78. Cowan, W. M., and P. G. H. Clarke. The development of the isthmo‐optic nucleus. Brain Behav. Evol. 13: 345–375, 1976.
 79. Cowan, W. M., J. W. Fawcett, D. D. M. O'Leary, and B. B. Stanfield. Regressive events in neurogenesis. Science Wash. DC 255: 1258–1265, 1984.
 80. Cowan, W. M., and D. M. O'Leary. Cell death and process elimination: the role of regressive phenomena in the development of the vertebrate nervous system. In: Medicine, Science, and Society: Symposia Celebrating The Harvard Medical School Bicentennial, edited by K. J. Isselbacher. New York: Wiley, 1984, p. 643–668.
 81. Cowey, A. Why are there so many visual areas? In: The Organization of the Cerebral Cortex, edited by F. O. Schmitt, F. G. Worden, G. Adelman, and S. G. Dennis. Cambridge, MA: MIT Press, 1981, p. 395–413.
 82. Craik, F. I. M. Age differences in human memory. In: The Handbook of the Psychology of Aging, edited by J. E. Birren and K. W. Schaie. New York: Van Nostrand Reinhold, 1977, p. 384–420.
 83. Crick, F. Memory and molecular turnover. Nature Lond. 312: 101, 1985.
 84. Crow, T. J., and S. Wendlandt. Impaired acquisition of a passive avoidance response after lesions induced in the locus coeruleus by 6‐OH‐dopamine. Nature Lond. 259: 42–44, 1976.
 85. Cummings, J. L., U. Tomiyasu, S. Read, and D. F. Benson. Amnesia with hippocampal lesions after cardiopulmonary arrest. Neurology 34: 679–681, 1984.
 86. Dahl, D., W. H. Bailey, and J. Winson. Effect of norepinephrine depletion of hippocampus on neuronal transmission from perforant pathway through dentate gyrus. J. Neurophysiol. 49: 123–133, 1983.
 87. Damasio, A. The frontal lobes. In: Clinical Neuropsychology, edited by K. M. Heilman and E. Valenstein. New York: Oxford Univ. Press, 1979, p. 360–412.
 88. Damasio, A. R., H. Damasio, and G. W. Van Hoesen. Prosopagnosia: anatomic basis and behavioral mechanisms. Neurology 32: 331–341, 1982.
 89. Damasio, A. R., N. R. Graff‐Radford, P. J. Eslinger, H. Damasio, and N. Kassell. Amnesia following basal forebrain lesions. Arch. Neurol. 42: 263–271, 1985.
 90. Davis, H. P., and L. R. Squire. Protein synthesis and memory: a review. Psychol. Bull. 96: 518–559, 1984.
 91. Davis, M., D. S. Gendelman, M. D. Tischler, and P. M. Gendelman. A primary acoustic startle circuit: lesion and stimulation studies. J. Neurosci. 2: 791–805, 1982.
 92. Davis, M., T. Parisi, D. S. Gendelman, M. Tischler, and J. H. Kehne. Habituation and sensitization of startle reflexes elicited electrically from the brainstem. Science Wash. DC 218: 688–689, 1982.
 93. Davis, W. J., and R. Gillette. Neural correlate of behavioral plasticity in command neurons of Pleurobranchaea. Science Wash. DC 199: 801–804, 1978.
 94. Daw, N. W., T. W. Robertson, R. K. Rader, T. O. Videen, and C. J. Coscia. Substantial reduction of cortical noradrenaline by lesions of adrenergic pathways does not prevent effects of monocular deprivation. J. Neurosci. 4: 1354–1360, 1984.
 95. De Groot, A. D. Het Denken van den Schaker. The Hague, The Netherlands: Mouton, 1965.
 96. (Thought and Choice in Chess. New York: Basic, 1965.)
 97. Denenberg, V. H., and R. W. Bell. Critical periods for the effects of infantile experience on adult learning. Science Wash. DC 131: 227–228, 1960.
 98. Desimone, R., and C. G. Gross. Visual areas in the temporal cortex of the macaque. Brain Res. 178: 363–380, 1979.
 99. Deutsch, J. A. The cholinergic synapse and the site of memory. Science Wash. DC 174: 788–794, 1971.
 100. De Wied, D. Influence of anterior pituitary on avoidance learning and escape behavior. Am. J. Physiol. 207: 255–259, 1964.
 101. De Wied, D., and W. H. Gispen. Behavioral effects of peptides. In: Peptides in Neurobiology, edited by H. Gainer. New York: Plenum, 1977, p. 397–448.
 102. Disterhoft, J. F., and J. S. Buchwald. Mapping learning in the brain. In: Biology of Reinforcement: Facets of Brain Stimulation Reward, edited by A. Routtenberg. New York: Academic, 1980, p. 53–80.
 103. Disterhoft, J. F., M. T. Shipley, and N. Kraus. Analyzing the rabbit NM conditioned reflex arc. In: Conditioning: Representation of Involved Neural Functions, edited by C. D. Woody. New York: Plenum, 1982, p. 433–449.
 104. Donegan, N. H., R. W. Lowry, and R. F. Thompson. Effects of lesioning cerebellar nuclei on conditioned leg‐flexion responses. Soc. Neurosci. Abstr. 9: 331, 1983.
 105. Drachman, D. A., and J. Arbit. Memory and the hippocampal complex. II. Is memory a multiple process? Arch. Neurol. 15: 52–61, 1966.
 106. Dunn, A. J. Neurochemistry of learning and memory: an evaluation of recent data. Annu. Rev. Psychol. 31: 343–390, 1980.
 107. Dunnett, S. B., W. C. Low, S. D. Iversen, U. Stenevi, and A. Björklund. Septal transplants restore maze learning in rats with fornix‐fimbria lesions. Brain Res. 251: 335–348, 1982.
 108. Durkovic, R. G., and D. H. Cohen. Effects of caudal midbrain lesions on conditioning of heart and respiratory rate responses in the pigeon. J. Comp. Physiol. Psychol. 69: 329–338, 1969.
 109. Eccles, J. C. The Neurophysiological Basis of Mind: The Principles of Neurophysiology. Oxford, UK: Clarendon, 1953.
 110. Eccles, J. C. The modular operation of the cerebral neocortex considered as the material basis of mental events. Neuroscience 6: 1839–1856, 1981.
 111. Eich, J. M. A composite holographic associative recall model. Psychol. Rev. 89: 627–661, 1982.
 112. Ericsson, K. A., W. G. Chase, and S. Faloon. Acquisition of a memory skill. Science Wash. DC 208: 1181–1182, 1980.
 113. Ferguson, S. M., M. Rayport, E. Gardner, W. Kass, H. Weiner, and M. F. Reiser. Similarities in mental content of psychotic states, spontaneous seizures, dreams, and responses to electrical brain stimulation in patients with temporal lobe epilepsy. Psychosom. Med. 31: 479–498, 1979.
 114. Ferrier, D. The Functions of the Brain. London: Smith, Elder, 1876.
 115. Fibiger, H. C. The organization and some projections of cholinergic neurons of the mammalian forebrain. Brain Res. Rev. 4: 327–388, 1982.
 116. Flexner, J. B., L. B. Flexner, and E. Stellar. Memory in mice as affected by intracerebral puromycin. Science Wash. DC 141: 57–59, 1963.
 117. Flourens, M. J. P. Recherches expérimentales sur les propriétés et les fonctions du système nerveux dans les animaux vertébrés. Paris: Ballière, 1824.
 118. Fodor, J. A. Modularity of Mind: Faculty Psychology. Cambridge, MA: MIT Press, 1983.
 119. Foletti, G., F. Regli, and G. Assal. Syndrome amnésique d'origine encéphalitique. Rev. Med. Suisse Romande 100: 179–185, 1980.
 120. Foote, S. L., F. E. Bloom, and G. Aston‐Jones. Nucleus locus ceruleus: new evidence of anatomical and physiological specificity. Physiol. Rev. 63: 844–914, 1983.
 121. Foote, S. L., and J. H. Morrison. Postnatal development of laminar innervation patterns by monoaminergic fibers in monkey (Macaca fascicularis) primary visual cortex J. Neurosci. 4: 2667–2680, 1984.
 122. Forbes, A., and C. S. Sherrington. Acoustic reflexes in the decerebrate cat. Am. J. Psychol. 35: 367–376, 1914.
 123. Freud, S. S. The Psychopathology of Everyday Life. London: Hogarth, 1901. (Standard Ed. 6.)
 124. Freud. S. S. Civilization and its Discontents. London: Hogarth, 1930. (Standard Ed. 21.)
 125. Fuster, J. M. Unit activity in prefrontal cortex during delayed‐response performance: neuronal correlates of transient memory. J. Neurophysiol. 36: 61–78, 1973.
 126. Fuster, J. M. The Prefrontal Cortex: Anatomy, Physiology, and Neuropsychology of the Frontal Lobe. New York: Raven, 1980.
 127. Fuster, J. M., and G. E. Alexander. Neuron activity related to short‐term memory. Science Wash. DC 173: 652–654, 1971.
 128. Fuster, J. M., and J. P. Jervey. Inferotemporal neurons distinguish and retain behaviorally relevant features of visual stimuli. Science Wash. DC 212: 952–955, 1981.
 129. Gabor, D. A new microscopic principle. Nature Lond. 161: 777–778, 1948.
 130. Gabor, D. Microscopy by reconstructed wavefronts. Pt. 2. Proc. R. Soc. Lond. B Biol. Sci. 64: 449–469, 1951.
 131. Gabriel, M., J. D. Miller, and S. E. Saltwick. Multiple‐unit activity of the rabbit medial geniculate nucleus in conditioning, extinction, and reversal. Physiol. Psychol. 4: 123–134, 1976.
 132. Gaffan, D. Recognition impaired and association intact in the memory of monkeys after transection of the fornix. J. Comp. Physiol. Psychol. 86: 1100–1109, 1974.
 133. Gaffan, D., R. C. Saunders, E. A. Gaffan, S. Harrison, C. Shields, and M. J. Owen. Effects of fornix transection upon associative memory in monkeys: role of the hippocampus in learned action. Q. J. Exp. Psychol. 36: 173–221, 1984.
 134. Gage, F. H., A. Björklund, U. Stenevi, S. B. Dunnett, and P. A. T. Kelley. Intrahippocampal septal grafts ameliorate learning impairments in aged rats. Science Wash. DC 225: 533–535, 1984.
 135. Gall, F. J. Sur les fonction du cerveau et sur celles de chacune des ses parties. Paris: Ballière, 1825, vol. 6, p. 1822–1825.
 136. Gallagher, M., and B. S. Kapp. Manipulation of opiate activity in the amygdala alters memory processes. Life Sci. 23: 1973–1978, 1978.
 137. Gallagher, M., R. A. King, and N. B. Young. Opiate antagonists improve spatial memory. Science Wash. DC 221: 975–976, 1983.
 138. Galton, F. Inquiries into Human Faculty and its Development. New York: Macmillan, 1883.
 139. Gardner, H. Frames of Mind: The Theory of Multiple Intelligences. New York: Basic, 1983.
 140. Gardner, H., F. Boller, J. Moreines, and N. Butters. Retrieving information from Korsakoff patients: effects of categorical cues and reference to the task. Cortex 9: 165–175, 1973.
 141. Gaze, R. M., M. J. Keating, G. Szekely, and L. Beazley. Binocular interaction in the formation of specific intertectal neuronal connexions. Proc. R. Soc. Lond. B Biol. Sci. 175: 107–147, 1970.
 142. Gerard, R. W. Physiology and psychiatry. Am. J. Psychiatry 105: 161–173, 1949.
 143. Ghent, L., M. Mishkin, and H. L. Teuber. Short‐term memory after frontal lobe injury in man. J. Comp. Physiol. Psychol. 55: 705–709, 1962.
 144. Gibbs, M., and K. T. Ng. Psychobiology of memory: towards a model of memory formation. Biobehav. Rev. 1: 113–136, 1977.
 145. Glanzer, M., and A. R. Cunitz. Two storage mechanisms in free recall. J. Verb. Learn. Verb. Behav. 5: 351–360, 1966.
 146. Glickman, S. E. Perseverative neural processes and consolidation of the memory trace. Psychol. Bull. 58: 218–233, 1961.
 147. Gloor, P., A. Olivier, L. F. Quesney, F. Andermann, and S. Horowitz. The role of the limbic system in experiential phenomena of temporal lobe epilepsy. Ann. Neurol. 12: 129–144, 1982.
 148. Gold, P. E., and R. L. Delanoy. ACTH modulation of memory storage processes. In: Endogenous Peptides and Learning and Memory Processes, edited by J. C. Martinez, Jr., R. A. Jensen, R. B. Messing, H. Rigter, and J. L. McGaugh. New York: Academic, 1981, p. 79–98.
 149. Gold, P. E., and J. L. McGaugh. A single‐trace, two‐process view of memory processes. In: Short‐Term Memory, edited by D. Deutsch and J. A. Deutsch. New York: Academic, 1975, p. 355–378.
 150. Gold, P. E., and R. Van Buskirk. Facilitation of time‐dependent memory processes with posttrial epinephrine injections. Behav. Biol. 13: 145–153, 1975.
 151. Gold, P. E., and R. Van Buskirk. Effects of posttrial hormone injections on memory processes. Horm. Behav. 7: 509–517, 1976.
 152. Gold, P. E., and R. Van Buskirk. Enhancement and impairment of memory processes with posttrial injections of adrenocorticotrophic hormone. Behav. Biol. 16: 387–400, 1976.
 153. Goldman, P. S., and W. J. H. Nauta. Columnar distribution of cortico‐cortical fibers in the frontal association, limbic, and motor cortex of the developing rhesus monkey. Brain Res. 122: 393–413, 1977.
 154. Goldman‐Rakic, P. S., and M. L. Schwartz. Interdigitation of contralateral and ipsilateral columnar projections to frontal association cortex in primates. Science Wash. DC 216: 755–757, 1982.
 155. Goltz, F. Über die Verrichtungen des Grosshirns. Pfluegers Arch. Gesamte Physiol. Menschen Tiere 13: 1–45; 14: 412–443; 20: 1–54; 26: 1–49; 1876–1884.
 156. Graf, P., and D. L. Schacter. Implicit and explicit memory for new associations in normal and amnesic subjects. J. Exp. Psychol. Learn. Mem. Cogn. 11: 501–518, 1985.
 157. Graf, P., A. P. Shimamura, and L. R. Squire. Priming across modalities and priming across category levels: extending the domain of preserved function in amnesia. J. Exp. Psychol. Learn. Med. Cogn. 11: 386–396, 1985.
 158. Graf, P., L. R. Squire, and G. Mandler. The information that amnesic patients do not forget. J. Exp. Psychol. Learn. Mem. Cogn. 10: 164–178, 1984.
 159. Graff‐Radford, N. R., P. J. Eslinger, A. R. Damasio, and T. Yamada. Nonhemorrhagic infarction of the thalamus: behavioral, anatomic and physiologic correlates. Neurology 34: 14–23, 1984.
 160. Green, E. J., W. T. Greenough, and B. E. Schlumpf. Effects of complex or isolated environments on cortical dendrites of middle‐aged rats. Brain Res. 264: 233–240, 1983.
 161. Greenough, W. T. Possible structural substrate of plastic neural phenomena. In: Neurobiology of Learning and Memory, edited by G. Lynch, J. L. McGaugh, and N. M. Weinberger. New York: Guilford, 1984, p. 470–478.
 162. Greenough, W. T. Structural correlates of information storage in the mammalian brain: a review and hypothesis. Trends Neurosci. 7: 229–233, 1984.
 163. Greenough, W. T., and F.‐L. F. Chang. Anatomically detectable correlates of information storage in the nervous systems of mammals. In: Neuronal Plasticity, edited by C. W. Cotman. New York: Guilford, 1985, p. 335–372.
 164. Grinnell, A. D. Specificity of neurons and their interconnections. In: Handbook of Physiology. The Nervous System, edited by J. M. Brookhart and V. B. Mountcastle. Bethesda, MD: Am. Physiol. Soc., 1977, sect. 1, vol. I, pt. 2, chapt. 22, p. 803–853.
 165. Gross, C. G. Comparison of the effects of partial and total lateral frontal lesions on test performance by monkeys. J. Comp. Physiol. Psychol. 56: 41–47, 1963.
 166. Gross, C. G. Visual functions of inferotemporal cortex. In: Handbook of Sensory Physiology. Central Processing of Visual Information, edited by R. Jung. Berlin: Springer‐Verlag, 1973, vol. 3, p. 451–452.
 167. Gross, C. G., D. B. Bender, and G. L. Gerstein. Activity of inferior temporal neurons in behaving monkeys. Neuropsychologia 17: 215–229, 1979.
 168. Gross, C. G., S. I. Chorover, and S. M. Cohen. Caudate, cortical, hippocampal and dorsal thalamic lesions in rats; alternation and Hebb‐Williams maze performance. Neuropsychologia 3: 53–68, 1965.
 169. Gross, C. G., C. E. Rocha‐Miranda, and D. B. Bender. Visual properties of neurons in inferotemporal cortex of the macaque. J. Neurophysiol. 35: 96–111, 1972.
 170. Groves, P. M., C. J. Wilson, and S. W. Miller. Habituation of the acoustic startle response: a neural systems analysis of habituation in the intact animal. In: Advances in Psychobiology, edited by A. H. Riesen and R. F. Thompson. New York: Wiley, 1976, vol. 3, p. 327–380.
 171. Gruner, J. E. Sur la pathologie des encéphalopathies alcooliques. Rev. Neurol. Paris 94: 682–689, 1956.
 172. Grunthal, E. Ueber das Corpus mamillare und den Korsakowschen Symtomen Komplex. Confin. Neurol. 2: 65–95, 1939.
 173. Gudden, H. Klinische und anatomische Beitrage zur Kenntnis der multiplen Alkoholneuritis nebst Bemerkungen über die Regenerationsvorgange im peripheren Nervensystem. Arch. Psychiatr. Nervenkr. 28: 643–741, 1896.
 174. Halgren, E. Human hippocampal and amygdala recording and stimulation: evidence for a neural model of recent memory. In: Neuropsychology of Memory, edited by L. R. Squire and N. Butters. New York: Guilford, 1984, p. 165–182.
 175. Halgren, E., R. D. Walter, D. G. Cherlow, and P. H. Crandall. Mental phenomena evoked by electrical stimulation of the human hippocampal formation and amygdala. Brain 101: 83–117, 1978.
 176. Hamburger, V. Cell death in the development of the lateral motor column of the chick embryo. J. Comp. Neurol. 160: 535–546, 1975.
 177. Hamilton, C. R., and M. S. Gazzaniga. Lateralization of learning of colour and brightness discriminations following brain bisection. Nature Lond. 201: 220, 1964.
 178. Hawkins, R. D., T. W. Abrams, T. J. Carew, and E. R. Kandel. A cellular mechanism of classical conditioning in Aplysia: activity‐dependent amplification of presynaptic facilitation. Science Wash. DC 219: 400–405, 1983.
 179. Hebb, D. O. The Organization of Behavior: A Neuropsychological Theory. New York: Wiley, 1949.
 180. Hebb, D. O. Neuropsychology: retrospect and prospect. Can. J. Psychol. 37: 4–7, 1983.
 181. Hecaen, H., and W. L. Albert. Human Neuropsychology. New York: Wiley, 1978.
 182. Hilgard, E. R., and D. G. Marquis. Conditioning and Learning. New York: Appleton‐Century‐Crofts, 1940.
 183. Hinton, G. E. Implementing semantic networks in parallel hardware. In: Parallel Models of Associative Memory, edited by G. E. Hinton and J. A. Anderson. Hillsdale, NJ: Erlbaum, 1981, p. 161–188.
 184. Hinton, G. E., and J. A. Anderson (editors). Parallel Models of Associative Memory. Hillsdale, NJ: Erlbaum, 1981.
 185. Hirsch, H. V. B., and D. N. Spinelli. Visual experience modifies distribution of horizontally and vertically oriented receptive fields in cats. Science Wash. DC 168: 869–871, 1970.
 186. Hirst, W. The amnesic syndrome: descriptions and explanations. Psychol. Bull. 91: 435–460, 1982.
 187. Hoffman, T. J., C. L. Sheridan, and D. M. Levinson. Interocular transfer in albino rats as a function of forebrain plus midbrain commissurotomy. Physiol. Behav. 27: 279–285, 1981.
 188. Horel, J. A. The neuroanatomy of amnesia: a critique of the hippocampal memory hypothesis. Brain 101: 403–445, 1978.
 189. Horn, G. Neural mechanisms of learning: an analysis of imprinting in the domestic chick. Proc. R. Soc. Lond. B Biol. Sci. 213: 101–137, 1981.
 190. Horn, G. Memory, Imprinting, and the Brain. Oxford, UK: Clarendon, 1985.
 191. Horn, G., B. J. McCabe, and J. Cipolla‐Neto. Imprinting in the domestic chick: the role of each side of the hyperstriatum ventrale in acquisition and retention. Exp. Brain Res. 53: 91–98, 1983.
 192. Horowitz, M. J., J. E. Adams, and B. B. Rutkin. Visual imagery on brain stimulation. Arch. Gen. Psychiatry 19: 469–486, 1968.
 193. Hoyle, G. Instrumental conditioning of the leg lift in the locust. Neurosci. Res. Program Bull. 17: 577–586, 1979.
 194. Hubel, D. H., and T. N. Wiesel. Receptive fields, binocular interaction, and functional architecture in the cat's visual cortex. J. Physiol. Lond. 160: 106–154, 1962.
 195. Hubel, D. H., and T. N. Wiesel. Binocular interaction in striate cortex of kittens reared with artificial squint. J. Neurophysiol. 28: 1041–1059, 1965.
 196. Hubel, D. H., T. N. Wiesel, and S. LeVay. Plasticity of ocular dominance columns in monkey striate cortex. Philos. Trans. R. Soc. Lond. B Biol. Sci. 278: 377–409, 1977.
 197. Hunt, T., T. Hunter, and A. Munro. Control of haemoglobin synthesis: rate of translation of the messenger RNA for the A and B chains. J. Mol. Biol. 43: 123–133, 1969.
 198. Hunter, W. S. The delayed reaction in animals and children. Behav. Monogr. 2: 1–86, 1913.
 199. Hunter, W. S. A consideration of Lashley's theory of the equipotentiality of cerebral action. J. Gen. Psychol. 3: 455–468, 1930.
 200. Huppert, F. A., and M. Piercy. Normal and abnormal forgetting in organic amnesia: effects of locus of lesion. Cortex 15: 385–390, 1979.
 201. Hyman, B. T., G. W. Van Hoesen, A. R. Damasio, and C. L. Barnes. Alzheimer's disease: cell specific pathology isolates the hippocampal formation. Science Wash. DC 225: 1168–1170, 1984.
 202. Ignelzi, R. J., and L. R. Squire. Recovery from anterograde and retrograde amnesia after percutaneous drainage of a cystic craniopharyngioma. J. Neurol. Neurosurg. Psychiatry 39: 1231–1235, 1976.
 203. Isseroff, A., H. E. Rosvold, T. W. Galkin, and P. S. Goldman‐Rakic. Spatial memory impairments following damage to the mediodorsal nucleus of the thalamus in rhesus monkeys. Brain Res. 232: 97–113, 1982.
 204. Ito, M. Cerebellar control of the vestibulo‐ocular reflex: around the flocculus hypothesis. Annu. Rev. Neurosci. 5: 275–296, 1982.
 205. Ito, M., and Y. Miyashita. The effect of chronic destruction of inferior olive upon visual modification of the horizontal vestibulo‐ocular reflex of rabbits. Proc. Jpn. Acad. 51: 716–760, 1975.
 206. Ito, M., T. Shiida, N. Yagi, and M. Yamamoto. Visual influence on rabbit horizontal vestibulo‐ocular reflex presumably effected via the cerebellar flocculus. Brain Res. 65: 170–174, 1974.
 207. Iversen, S. D. Brain lesions and memory in animals: a reappraisal. In: The Physiological Basis of Memory, edited by J. A. Deutsch. New York: Academic, 1973, p. 139–198.
 208. Iwai, E., and M. Mishkin. Two visual foci in the temporal lobe of monkeys. In: Neurophysiological basis of Learning and Behavior, edited by N. Yoshii and N. A. Buchwald. Osaka, Japan: Osaka Univ. Press, 1968, p. 1–11.
 209. Izquierdo, I. Effect of naloxone and morphine on various forms of memory in the rat: possible role of endogenous opiate mechanisms in memory consolidation. Psychopharmacology 66: 199–203, 1979.
 210. Jacobsen, C. F. Functions of the frontal association area in primates. Arch. Neurol. Psychiatry 33: 558–569, 1935.
 211. Jacobsen, C. F. Studies of cerebral function in primates. I. The functions of the frontal association areas in monkeys. Comp. Psychol. Monogr. 13: 3–60, 1936.
 212. Jacobsen, C. F., and H. W. Nissen. Studies of cerebral function in primates. IV. The effects of frontal lobe lesions on the delayed alternation habit in monkeys. J. Comp. Physiol. Psychol. 23: 101–112, 1937.
 213. Jacoby, L. L., and M. Dallas. On the relationship between autobiographical memory and perceptual learning. J. Exp. Psychol. Gen. 110: 306–340, 1981.
 214. Jacoby, L. L., and D. Witherspoon. Remembering without awareness. Can. J. Psychol. 32: 300–324, 1982.
 215. James, W. The Principles of Psychology. New York: Holt, 1890.
 216. Jenkins, W. M., and M. M. Merzenich. Reorganization of neocortical representations after brain injury: a neurophysiological model of the bases of recovery from stroke. In: Progress in Brain Research, edited by F. Seil, E. Herbert, and B. Carlson. Amsterdam: Elsevier, in press.
 217. Jenkins, W. M., M. M. Merzenich, and M. T. Ochs. Behaviorally controlled differential use of restricted hand surfaces induce changes in area 3b of owl monkeys. Soc. Neurosci. Abstr. 10: 665, 1984.
 218. John, E. R. Switchboard versus statistical theories of learning and memory. Science Wash. DC 177: 850–864, 1972.
 219. John, E. R., F. Bartlett, M. Shimokochi, and D. Kleinman. Neural readout from memory. J. Neurophysiol. 36: 893–924, 1973.
 220. John, E. R., and P. P. Morgades. Neural correlates of conditioned responses studied with multiple chronically implanted moving microelectrodes. Exp. Neurol. 23: 412–425, 1969.
 221. John, E. R., and E. L. Schwartz. The neurophysiology of information processing and cognition. Annu. Rev. Psychol. 29: 1–29, 1978.
 222. Jones, E. G., and T. P. S. Powell. An anatomical study of converging sensory pathways within the cerebral cortex of the monkey. Brain 93: 793–820, 1970.
 223. Jones, G. M. Plasticity in the adult vestibulo‐ocular reflex arc. Philos. Trans. R. Soc. Lond. B Biol. Sci. 278: 319–334, 1977.
 224. Juraska, J. M., W. T. Greenough, C. Elliott, K. J. Mack, and R. Berkowitz. Plasticity in adult rat visual cortex: an examination of several cell populations after differential rearing. Behav. Neural Biol. 29: 157–167, 1980.
 225. Kahn, E. A., and E. C. Crosby. Korsakoff's syndrome associated with surgical lesions involving the mammillary bodies. Neurology 22: 117–125, 1972.
 226. Kandel, E. R. Cellular Basis of Behavior: An Introduction to Behavioral Neurobiology. San Francisco, CA: Freeman, 1976.
 227. Kandel, E. R. Neuronal plasticity and the modification of behavior. In: Handbook of Physiology. The Nervous System, edited by J. M. Brookhart and V. B. Mountcastle. Bethesda, MD: Am. Physiol. Soc., 1977, sect. 1, vol. I, pt. 2, chapt. 29, p. 1137–1182.
 228. Kandel, E. R. From metapsychology to molecular biology: explorations into the nature of anxiety. Am. J. Psychiatry 140: 1277–1293, 1983.
 229. Kandel, E. R., and J. H. Schwartz. Molecular biology of learning: modification of transmitter release. Science Wash. DC 218: 433–442, 1982.
 230. Kandel, E. R., and W. A. Spencer. Cellular neurophysiological approaches in the study of learning. Physiol. Rev. 48: 65–134, 1968.
 231. Kapp, B. S., R. C. Frysinger, M. Gallagher, and J. R. Haselton. Amygdala central nucleus lesions: effect on heart rate conditioning in the rabbit. Physiol. Behav. 23: 1109–1117, 1979.
 232. Kapp, B. S., M. Gallagher, C. D. Applegate, and R. C. Frysinger. The amygdala central nucleus: contributions to conditioned cardiovascular responding during aversive Pavlovian conditioning in the rabbit. In: Conditioning: Representation of Involved Neural Functions, edited by C. D. Woody. New York: Plenum, 1982, vol. 26, p. 581–598.
 233. Kasamatsu, T. Neuronal plasticity maintained by the central norepinephrine system in the cat visual cortex. Prog. Psychobiol. Physiol. Psychol. 10: 1983, 1–83.
 234. Kesner, R. P., and J. M. Novak. Serial position curve in rats: role of the dorsal hippocampus. Science Wash. DC 218: 173–175, 1982.
 235. Kesner, R. P., and M. W. Wilburn. A review of electrical stimulation of the brain in context of learning and retention. Behav. Biol. 10: 259–293, 1974.
 236. Kettner, R. E., and R. E. Thompson. Auditory signal detection and decision processes in the nervous system. J. Comp. Physiol. Psychol. 96: 328–331, 1982.
 237. Kinsbourne, M., and F. Wood. Short‐term memory processes and the amnesic syndrome. In: Short‐Term Memory, edited by D. Deutsch and J. A. Deutsch. New York: Academic, 1975, p. 258–291.
 238. Klapp, S. T., E. A. Marshburn, and P. T. Lester. Short‐term memory does not involve the “working memory” of information processing: the demise of a common assumption. J. Exp. Psychol. Gen. 112: 240–264, 1983.
 239. Klüver, H. Functional significance of the geniculo‐striate system. In: Visual Mechanisms, edited by H. Klüver. Lancaster, PA: Cattell, 1942, p. 253–299.
 240. Koffka, K. Principles of Gestalt Psychology. New York: Harcourt, Brace, 1935.
 241. Kohler, W. Dynamics in Psychology. New York: Liveright, 1940.
 242. Kohler, W. Gestalt Psychology: An Introduction to New Concepts in Modern Psychology. New York: Liveright, 1947.
 243. Konishi, M. A logical basis for single‐neuron study of learning in complex neural systems. In: The Biology of Learning, edited by P. Marler and H. S. Terrace. Berlin: Springer‐Verlag, 1984, p. 311–324. (Dahlem Konferenzen.)
 244. Konishi, M. Birdsong: from behavior to neuron. Annu. Rev. Neurosci. 8: 125–170, 1985.
 245. Konorski, J. Conditioned Reflexes and Neuron Organization. Cambridge, UK: Cambridge Univ. Press, 1948.
 246. Korsakoff, S. S. Disturbance of psychic function in alcoholic paralysis and its relation to the disturbance of the psychic sphere in multiple neuritis of non‐alcoholic origin. Vestn. Psychiatr. 4: fascicle 2, 1887.
 247. Kovner, R., and J. S. Stamm. Disruption of short‐term visual memory by electrical stimulation of inferotemporal cortex in the monkey. J. Comp. Physiol. Psychol. 81: 163–172, 1972.
 248. Kowalska, D. M., J. Bachevalier, and M. Mishkin. Inferior prefrontal cortex and recognition memory. Soc. Neurosci. Abstr. 10: 385, 1984.
 249. Krasne, F. B. Extrinsic control of intrinsic neuronal plasticity: an hypothesis from work on simple systems. Brain Res. 140: 197–216, 1978.
 250. Lashley, K. S. Brain Mechanisms and Intelligence. A Quantitative Study of Injuries to the Brain. Chicago, IL: Chicago Univ. Press, 1929.
 251. Lashley, K. S. In search of the engram. In: The Neuropsychology of Lashley, edited by F. A. Beach, D. O. Hebb, C. T. Morgan, and H. W. Nissen. New York: McGraw‐Hill, 1960, p. 454–482.
 252. Lashley, K. S., K. L. Chow, and J. Semmes. An examination of the electrical field theory of cerebral integration. Psychol. Rev. 58: 123–136, 1951.
 253. Lavond, D. G., T. L. Hembree, and R. F. Thompson. Effect of kainic acid lesions of the cerebellar interpositus nucleus on eyelid conditioning in the rabbit. Brain Res. 326: 179–182, 1985.
 254. LeDoux, J. E., A. Sakaguchi, and D. J. Reis. Subcortical efferent projections of the medial geniculate nucleus mediate emotional responses conditioned to acoustic stimuli. J. Neurosci. 4: 683–698, 1984.
 255. Lee, K., F. Schottler, M. Oliver, and G. Lynch. Brief bursts of high‐frequency stimulation produce two types of structural change in rat hippocampus. J. Neurophysiol. 44: 247–258, 1980.
 256. Lehmann, J., J. I. Nagy, S. Atmadia, and H. C. Fibiger. The nucleus basalis magnocellularis: the origin of a cholinergic projection to the neocortex of the rat. Neuroscience 5: 1161–1174, 1980.
 257. Lehtonen, R. Learning, memory and intellectual performance in a chronic state of amnesic syndrome. Acta Psychiatr. Neurol. Scand. Suppl. 54: 1–156, 1973.
 258. Leith, E. N., and J. Upatnicks. Reconstructed wavefronts and communication theory. J. Opt. Soc. Am. 52: 1123–1130, 1962.
 259. LeVay, S., and M. P. Stryker. The development of ocular dominance columns in the cat. Soc. Neurosci. Symp. 4: 83–98, 1979.
 260. LeVay, S., M. P. Stryker, and C. J. Schatz. Ocular dominance columns and their development in layer IV of the cat's visual cortex. A quantitative study. J. Comp. Neurol. 179: 223–244, 1978.
 261. LeVay, S., T. N. Wiesel, and D. H. Hubel. The development of ocular dominance columns in normal and visually deprived monkeys. J. Comp. Neurol. 191: 1–51, 1980.
 262. Lichtman, J. W. Reorganisation of synaptic connexions in the rat submandibular ganglion during postnatal development. J. Physiol. Lond. 273: 155–177, 1977.
 263. Lindvall, O., and A. Björklund. Organization of catecholamine neurons in the rat central nervous system. In: Handbook of Psychopharmacology. Chemical Pathways in the Brain, edited by L. L. Iversen, S. D. Iversen, and S. H. Snyder. New York: Plenum, 1978, vol. 9, p. 139–231.
 264. Lisman, J. E. A mechanism for memory storage insensitive to molecular turnover: bistable autophosphorylating kinase. Proc. Natl. Acad. Sci. USA 82: 3055–3057, 1985.
 265. Livingston, R. B. Reinforcement. In: The Neurosciences: A Study Program, edited by G. C. Quarton, T. Melnechuk, and F. O. Schmitt. New York: Rockefeller Univ. Press, 1967, p. 568–576.
 266. Livingstone, M. S., and D. H. Hubel. Anatomy and physiology of a color system in the primate visual cortex. J. Neurosci. 4: 309–356, 1984.
 267. Loftus, E. F., and G. R. Loftus. On the permanence of stored information in the human brain. Am. Psychol. 35: 49–72, 1980.
 268. Lorente de Nó, R. Cerebral cortex: architecture, intracortical connections, motor projections. In: Physiology of the Nervous System, edited by J. F. Fulton. New York: Oxford Univ. Press, 1938, p. 291–339.
 269. Lugaro, E. I recenti progressi déll'anatomia del sistema nervoso in rapporto alla psicologia ed alla psichiatria. Riv. Sper. Freniatr. Med. Leg. Alienazioni Ment. 26: 831–894, 1900. [Cited in Ramón y Cajal (381b).]
 270. Luria, A. R. Higher Cortical Functions in Man. London: Tavistock, 1966.
 271. Luria, A. R. Frontal‐lobe syndromes. In: Handbook of Clinical Neurology. Localization in Clinical Neurology, edited by P. J. Vinken and G. W. Bruyn. Amsterdam: Elsevier/North‐Holland, 1969, vol. 2, p. 725–757.
 272. Luria, A. R. The Working Brain: An Introduction to Neuropsychology. New York: Basic, 1973.
 273. Lynch, G., and M. Baudry. The biochemistry of memory: a new and specific hypothesis. Science Wash. DC 224: 1057–1063, 1984.
 274. Mahl, G. F., A. Rothenberg, J. M. R. Delgago, and H. Hamlin. Psychological responses in the human to intracerebral electrical stimulation. Psychosom. Med. 26: 337–368, 1964.
 275. Mahut, H., M. Moss, and S. Zola‐Morgan. Retention deficits after combined amygdala‐hippocampal and selective hippocampal resections in the monkey. Neuropsychologia 19: 201–225, 1981.
 276. Mahut, H., S. Zola‐Morgan, and M. Moss. Hippocampal resections impair associative learning and recognition memory in the monkey. J. Neurosci. 2: 1214–1229, 1982.
 277. Mair, W. G. P., E. K. Warrington, and L. Weiskrantz. Memory disorder in Korsakoff psychosis. A neuropathological and neuropsychological investigation of two cases. Brain 102: 749–783, 1979.
 278. Malamud, N., and S. A. Skillicorn. Relationship between the Wernicke and Korsakoff syndrome: a clinicopathologic study of seventy cases. Arch. Neurol. Psychiatry 76: 585–596, 1956.
 279. Mandler, G. Organization and repetition: organizational principles with special reference to rote learning. In: Perspectives on Memory Research, edited by L. G. Nilsson. Hillsdale, NJ: Erlbaum, 1979, p. 293–327.
 280. Mandler, G. Recognizing: the judgment of previous occurrence. Psychol. Rev. 87: 252–271, 1980.
 281. Mandler, J. Representation and recall in infancy. In: Infant Memory, edited by M. Moscovitch. New York: Plenum, 1984, p. 75–101.
 282. Markowitsch, H. J. Thalamic mediodorsal nucleus and memory: a critical evaluation of studies in animals and man. Neurosci. Biobehav. Rev. 6: 351–380, 1982.
 283. Marler, P. Song learning: innate species differences in the learning process. In: The Biology of Learning, edited by P. Marler and H. Terrace. Berlin: Springer‐Verlag, 1984, p. 289–309. (Dahlem Konferenzen.)
 284. Marr, D. A theory of cerebellar cortex. J. Physiol. Lond. 202: 437–470, 1969.
 285. Marslen‐Wilson, W. D., and H. L. Teuber. Memory for remote events in anterograde amnesia: recognition of public figures from newsphotographs. Neuropsychologia 13: 353–364, 1975.
 286. Martinez, J. L., Jr., R. A. Jensen, R. B. Messing, H. Rigter, and J. L. McGaugh (editors). Endogenous Peptides and Learning and Memory Processes. New York: Academic, 1981, p. 587.
 287. Martinez, J. L., Jr., R. A. Jensen, R. B. Messing, B. J. Vasquez, B. Soumireu‐Mourat, D. Geddes, K. C. Liang, and J. L. McGaugh. Central and peripheral actions of amphetamine on memory storage. Brain Res. 182: 157–166, 1980.
 288. Martinez, J. L., Jr., B. J. Vasquez, H. Rigter, R. B. Messing, R. A. Jensen, K. C. Liang, and J. L. McGaugh. Attenuation of amphetamine‐induced enhancement of learning by adrenal demedullation. Brain Res. 195: 433–443, 1980.
 289. Mason, S. T. Noradrenaline in the brain: progress in theories of behavioural function. Prog. Neurobiol. 16: 263–303, 1981.
 290. Mayes, A., and P. Meudell. Amnesia in humans and other animals. In: Memory in Animals and Humans, edited by A. Mayes. Wokingham, UK: Van Nostrand Reinhold, 1983, p. 203–252.
 291. McCabe, B. J., J. Cipolla‐Neto, G. Horn, and P. Bateson. Amnesic effects of bilateral lesions in the hyperstriatum ventrale of the chick after imprinting. Exp. Brain Res. 48: 13–21, 1982.
 292. McCabe, B. J., G. Horn, and P. P. G. Bateson. Effects of restricted lesions of the chick forebrain on the acquisition of filial preferences during imprinting. Brain Res. 205: 29–37, 1981.
 293. McCormick, D. A., G. A. Clark, D. G. Lavond, and R. F. Thompson. Initial localization of the memory trace for a basic form of learning. Proc. Natl. Acad. Sci. USA 79: 2731–2735, 1982.
 294. McCormick, D. A., J. E. Steinmetz, and R. F. Thompson. Lesions of the inferior olivary complex cause extinction of the classically conditioned eyeblink response. Brain Res. 359: 120–130, 1985.
 295. McCormick, D. A., and R. F. Thompson. Locus coeruleus lesions and resistance to extinction of a classically conditioned response: involvement of the neocortex and hippocampus. Brain Res. 245: 239–249, 1982.
 296. McCormick, D. A., and R. F. Thompson. Cerebellum: essential involvement in the classically conditioned eyelid response. Science Wash. DC 223: 296–299, 1984.
 297. McEntee, W. J., M. P. Biber, D. P. Perl, and F. D. Benson. Diencephalic amnesia: a reappraisal. J. Neurol. Neurosurg. Psychiatry 39: 436–441, 1976.
 298. McGaugh, J. L. Drug facilitation of learning and memory. Annu. Rev. Pharmacol. 13: 229–241, 1973.
 299. McGaugh, J. L. Hormonal influences on memory. Annu. Rev. Psychol. 34: 297–323, 1983.
 300. McGaugh, J. L. Preserving the presence of the past: hormonal influences on memory storage. Am. Psychol. 38: 161–174, 1983.
 301. McGaugh, J. L., and P. E. Gold. Modulation of memory by electrical stimulation of the brain. In: Neural Mechanisms of Learning and Memory, edited by M. R. Rosenzweig and E. L. Bennett. Cambridge, MA: MIT Press, 1976, p. 549–560.
 302. McGaugh, J. L., and M. J. Herz. Memory Consolidation. San Francisco, CA: Albion, 1972.
 303. McGeoch, J. A. The Psychology of Human Learning: An Introduction (1st ed.). New York: Longmans, Green, 1942.
 304. McKinney, M., R. G. Struble, D. L. Price, and T. Coyle. Monkey nucleus basalis is enriched with choline acetyltransferase. Neuroscience 10: 2363–2368, 1982.
 305. McNaughton, B. L. Long‐term synaptic enhancement and short‐term potentiation in rat fascia dentata act through different mechanisms. J. Physiol. Lond. 324: 249–262, 1982.
 306. Meadows, J. C. The anatomical basis of prosopagnosia. J. Neurol. Neurosurg. Psychiatry 37: 489–501, 1974.
 307. Meikle, T. H. Failure of interocular transfer of brightness discrimination. Nature Lond. 202: 1243–1244, 1964.
 308. Meikle, T. H., and J. A. Sechzer. Interocular transfer of brightness discrimination in “split‐brain” cats. Science Wash. DC 132: 734–735, 1960.
 309. Merzenich, M. M., and J. H. Kaas. Principles of organization of sensory‐perceptual systems in mammals. Prog. Psychobiol. Physiol. Psychol. 9: 1–42, 1980.
 310. Merzenich, M. M., J. H. Kaas, J. T. Wall, M. Sur, R. J. Nelson, and D. J. Fellman. Progression of change following median nerve section in the cortical representation of the hand in areas 3b and 1 in adult owl and squirrel monkeys. Neuroscience 3: 639–665, 1983.
 311. Mesulam, M., and G. W. Van Hoesen. Acetylcholinesterase‐rich projections from the basal forebrain of the rhesus monkey to neocortex. Brain Res. 109: 152–157, 1976.
 312. Meudell, P. R., B. Northern, J. S. Snowden, and D. Neary. Long‐term memory for famous voices in amnesic and normal subjects. Neuropsychologia 18: 133–139, 1980.
 313. Meyer, D. R., and P. M. Meyer. Dynamics and bases of recoveries of functions after injuries to the cerebral cortex. Physiol. Psychol. 5: 133–165, 1977.
 314. Michel, D., B. Laurent, N. Foyatier, A. Blanc, and M. Portafix. Infarctus thalamique paramédian gauche. Etude de la mémoire et du langage. Rev. Neurol. Paris 138: 533–550, 1982.
 315. Miles, F. A., and S. G. Lisberger. Plasticity in the vestibuloocular reflex: a new hypothesis. Annu. Rev. Neurosci. 4: 273–300, 1981.
 316. Miller, G. A. The magical number seven: plus or minus two. Some limits on our capacity for processing information. Psychol. Rev. 9: 81–97, 1956.
 317. Miller, N. E. Certain facts of learning relevant to the search for its physical basis. In: The Neurosciences: A Study Program, edited by G. C. Quarton, T. Melnechuk, and F. O. Schmitt. New York: Rockefeller Univ. Press, 1967, p. 643–652.
 318. Miller, R. R., and N. A. Marlin. The physiology and semantics of consolidation. In: Memory Consolidation: Towards a Psychobiology of Cognition, edited by H. Weingartner and E. Parker. Hillsdale, NJ: Erlbaum, 1984, p. 85–110.
 319. Miller, R. R., and A. D. Springer. Amnesia, consolidation, and retrieval. Psychol. Rev. 80: 69–79, 1973.
 320. Mills, R. P., and P. D. Swanson. Vertical oculomotor apraxia and memory loss. Ann. Neurol. 4: 149–153, 1976.
 321. Milner, B. Les troubles de la mémoire accompagnant des lesions hippocampiques bilaterales. In: Physiologie de l'hippocampe. Paris: CNRS, 1962, p. 257–272.
 322. Milner, B. Effects of different brain lesions on card sorting. Arch. Neurol. 9: 90–100, 1963.
 323. Milner, B. Some effects of frontal lobectomy in man. In: The Frontal Granular Cortex and Behavior, edited by J. M. Warren and K. Akert. New York: McGraw‐Hill, 1964, p. 313–334.
 324. Milner, B. Brain mechanisms suggested by studies of temporal lobes. In: Brain Mechanisms Underlying Speech and Language, edited by F. L. Darley. New York: Grune & Stratton, 1967, p. 122–145.
 325. Milner, B. Interhemispheric differences in the localisation of psychological processes in man. Br. Med. Bull. 27: 272–277, 1971.
 326. Milner, B. Disorders of learning and memory after temporal lobe lesions in man. Clin. Neurosurg. 19: 421–446, 1972.
 327. Milner, B. Hemispheric specialization: scope and limits. In: The Neurosciences: Third Study Program, edited by F. O. Schmitt and F. G. Worden. Cambridge, MA: MIT Press, 1974, p. 75–89.
 328. Milner, B. Clues to the cerebral organization of memory. In: Cerebral Correlates of Conscious Experience, edited by P. A. Buser and A. Rougeul‐Buser. Amsterdam: Elsevier/North‐Holland, 1978, p. 139–153.
 329. Milner, B. Some cognitive effects of frontal‐lobe lesions in man. Philos. Trans. R. Soc. Lond. B Biol. Sci. 298: 211–226, 1982.
 330. Mishkin, M. Effects of small frontal lesions on delayed alternation in monkeys. J. Neurophysiol. 20: 615–622, 1957.
 331. Mishkin, M. Visual mechanisms beyond the striate cortex. In: Frontiers in Physiological Psychology, edited by R. Russell. New York: Academic, 1966, p. 93–119.
 332. Mishkin, M. Cortical visual areas and their interaction. In: The Brain and Human Behavior, edited by A. G. Karczmar and J. C. Eccles. Berlin: Springer‐Verlag, 1972, p. 187–208.
 333. Mishkin, M. Memory in monkeys severely impaired by combined but not by separate removal of amygdala and hippocampus. Nature Lond. 273: 297–298, 1978.
 334. Mishkin, M. Analogous neural models for tactual and visual learning. Neuropsychologia 17: 139–151, 1979.
 335. Mishkin, M. A memory system in the monkey. Philos. Trans. R. Soc. Lond. B Biol. Sci. 298: 85–95, 1982.
 336. Mishkin, M., and J. Bachevalier. Object recognition impaired by ventromedial but not dorsolateral prefrontal cortical lesions in monkeys. Soc. Neurosci. Abstr. 9: 29, 1983.
 337. Mishkin, M., and J. Delacour. An analysis of short‐term visual memory in the monkey. J. Exp. Psychol. Anim. Behav. Processes 1: 326–334, 1975.
 338. Mishkin, M., B. Malamut, and J. Bachevalier. Memories and habits: two neural systems. In: Neurobiology of Learning and Memory, edited by G. Lynch, J. L. McGaugh, and N. M. Weinberger. New York: Guilford, 1984, p. 65–77.
 339. Mishkin, M., and F. J. Manning. Nonspatial memory after selective prefrontal lesions in monkeys. Brain Res. 143: 313–323, 1978.
 340. Mishkin, M., B. J. Spiegler, R. C. Saunders, and B. J. Malamut. An animal model of global amnesia. In: Alzheimer's Disease: A Report of Progress in Research, edited by S. Corkin, K. L. Davis, J. H. Growdon, E. Usdin, and R. J. Wurtman. New York: Raven, 1982, p. 235–247.
 341. Mishkin, M., B. Vest, M. Waxler, and H. E. Rosvold. A re‐examination of the effects of frontal lesions on object alternation. Neuropsychologia 7: 357–363, 1969.
 342. Monsell, S. Components of working memory underlying verbal skills: a “distributed capacities” view. In: International Symposium on Attention and Peformance, edited by H. Bouma and D. Bouwhuis. Hillsdale, NJ: Erlbaum, 1984, vol. 10, p. 327–350.
 343. Moore, J. W., C. H. Yeo, D. A. Oakley, and I. S. Russell. Conditioned inhibition of the nictitating membrane response in neodecorticate rabbits. Behav. Brain Res. 1: 397–410, 1980.
 344. Moore, R. Y., and F. E. Bloom. Central catecholamine neuron systems: anatomy and physiology of the dopamine systems. Annu. Rev. Neurosci. 1: 129–169, 1978.
 345. Moore, R. Y., and F. E. Bloom. Central catecholamine neuron systems: anatomy and physiology of the norepinephrine and epinephrine systems. Annu. Rev. Neurosci. 2: 113–168, 1979.
 346. Morris, R. G. M., P. Garrud, J. N. P. Rawlins, and J. O'Keefe. Place navigation impaired in rats with hippocampal lesions. Nature Lond. 297: 681–683, 1982.
 347. Morrison, J. H., M. E. Molliver, and R. Grzanna. Noradrenergic innervation of cerebral cortex: widespread effects of local cortical lesions. Science Wash. DC 205: 313–316, 1979.
 348. Moscovitch, M. Multiple dissociations of function in amnesia. In: Human Memory and Amnesia, edited by L. Cermak. Hillsdale, NJ: 1982, p. 337–370.
 349. Moss, M., H. Mahut, and S. Zola‐Morgan. Concurrent discrimination learning of monkeys after hippocampal, entorhinal, or fornix lesions. J. Neurosci. 1: 227–240, 1981.
 350. Mountcastle, V. B. Modality and topographic properties of single neurons of cat's somatic sensory cortex. J. Neurophysiol. 20: 408–434, 1957.
 351. Mountcastle, V. B. An organizing principle for cerebral function: the unit module and the distributed system. In: The Neurosciences: Fourth Study Program, edited by F. O. Schmitt and F. G. Worden. Cambridge, MA: MIT Press, 1979, p. 21–42.
 352. Müller, G. E., and A. Pilzecker. Experimentelle Beitrage zur Lehre vom Gedachtniss [Experimental contributions to the theory of memory]. Z. Psychol. 1: 1–288, 1900.
 353. Murdock, B. B. A theory for the storage and retrieval of item and associative information. Psychol. Rev. 89: 609–626, 1982.
 354. Murray, E. A., and M. Mishkin. Amygdalectomy impairs crossmodal association in monkeys. Science Wash. DC 228: 604–606, 1985.
 355. Nadel, L., and S. Zola‐Morgan. Toward the understanding of infant memory: contributions from animal neuropsychology. In: Infant Memory, edited by M. Moscovitch. New York: Plenum, 1984, p. 145–172.
 356. Nakamura, R. K., and M. Mishkin. Chronic blindness following nonvisual lesions in monkeys: partial lesions and disconnection effects. Soc. Neurosci. Abstr. 8: 812, 1982.
 357. Neisser, U. Cognitive Psychology. New York: Appleton‐Centry‐Crofts, 1967.
 358. Nottebohm, F. Brain pathways for vocal learning in birds: a review of the first 10 years. Prog. Psychobiol. Physiol. Psychol. 7: 86–120, 1980.
 359. Nottebohm, F. A brain for all seasons: cyclical anatomical changes in song control nuclei of the canary brain. Science Wash. DC 214: 1368–1370, 1981.
 360. Oakley, D. A., and I. S. Russell. Neocortical lesions and classical conditioning. Physiol. Behav. 8: 915–926, 1972.
 361. Ojemann, G. A. Brain organization for language from the perspective of electrical stimulation mapping. Behav. Brain Sci. 6: 189–230, 1983.
 362. O'Keefe, J., and L. Nadel. The Hippocampus as a Cognitive Map. London: Oxford Univ. Press, 1978.
 363. Olton, D. S., J. T. Becker, and G. E. Handelmann. Hippocampus, space, and memory. Behav. Brain Sci. 2: 313–365, 1979.
 364. Papez, J. W. A proposed mechanism of emotion. Arch. Neurol. Psychiatry 38: 725–743, 1937.
 365. Parkin, A. J. Residual learning capability in organic amnesia. Cortex 18: 417–440, 1982.
 366. Parkin, A. J. Amnesic syndrome: a lesion‐specific disorder? Cortex 20: 479–508, 1984.
 367. Pasik, P., and T. Pasik. Visual functions in monkeys after total removal of visual cerebral cortex. In: Contributions to Sensory Physiology, edited by W. D. Neff. New York: Academic, 1982, vol. 7, p. 147–200.
 368. Passingham, R. E. Delayed matching after selective prefrontal lesions in monkeys (Macaca mulatta). Brain Res. 92: 89–102, 1975.
 369. Patterson, M. M. Mechanisms of classical conditioning of spinal reflexes. In: Neural Mechanisms of Goal‐Directed Behavior and Learning, edited by R. F. Thompson, L. H. Hicks, and V. B. Shvyrokov. New York: Academic, 1980, p. 263–272.
 370. Peck, C. K., S. G. Crewther, and C. R. Hamilton. Partial interocular transfer of brightness and movement discrimination by split‐brain cats. Brain Res. 163: 61–75, 1979.
 371. Penfield, W. The Excitable Cortex in Conscious Man. Springfield, IL: Thomas, 1958.
 372. Penfield, W. W., and H. Jasper. Epilepsy and the Functional Anatomy of the Human Brain. Boston, MA: Little, Brown, 1954.
 373. Penfield, W., and G. Mathieson. Memory: autopsy findings and comments on the role of hippocampus in experiential recall. Arch. Neurol. 31: 145–154, 1974.
 374. Penfield, W., and B. Milner. Memory deficit produced by bilateral lesions in the hippocampal zone. Arch. Neurol. Psychiatry 79: 475–497, 1958.
 375. Penfield, W., and P. Perot. The brain's record of auditory and visual experience. Brain 86: 595–696, 1963.
 376. Petrides, M. Motor conditional associative‐learning after selective prefrontal lesions in the monkey. Behav. Brain Res. 5: 407–413, 1982.
 377. Petrides, M., and B. Milner. Deficits on subject‐ordered tasks after frontal‐ and temporal‐lobe lesions in man. Neuropsychologia 20: 249–262, 1982.
 378. Powell, P. A., M. Lipkin, and W. L. Milligan. Concomitant changes in classically conditioned heart rate and corneoretinal potential discrimination in the rabbit (Oryctolagus cuniculus). Learn. Motiv. 5: 532–547, 1974.
 379. Pribram, K. H. Neurophysiology and learning. I. Memory and the organization of attention. In: Brain Function. Brain Function and Learning, edited by D. B. Lindsley and A. A. Lumsdaine. Berkeley: Univ. of California Press, 1964, vol. 4, p. 79–112.
 380. Pribram, K. H. Languages of the Brain: Experimental Paradoxes and Principles in Neuropsychology. Englewood Cliffs, NJ: Prentice‐Hall, 1971.
 381. Pribram, K. H., M. Nuwer, and R. J. Baron. The holographic hypothesis of memory structure in brain function and perception. In: Contemporary Developments in Mathematical Psychology. Measurement, Psychophysics, and Neural Information Processing, edited by D. H. Krantz, R. C. Atkinson, R. D. Luce, and P. Suppes. San Francisco, CA: Freeman, 1974, vol. 2, p. 416–457.
 382. Prosser, C. L., and W. S. Hunter. The extinction of startle responses and spinal reflexes in the white rat. Am. J. Physiol. 117: 609–618, 1936.
 383. Purves, D. Modulation of neuronal competition by postsynaptic geometry in autonomic ganglia. Trends Neurosci. 6: 10–16, 1983.
 384. Purves, D., and J. W. Lichtman. Elimination of synapses in the developing nervous system. Science Wash. DC 210: 153–157, 1980.
 385. Quinn, W. G., and R. J. Greenspan. Learning and courtship in Drosophila: two stories with mutants. Annu. Rev. Neurosci. 7: 67–94, 1984.
 386. Rakic, P. Prenatal development of the visual system in rhesus monkey. Philos. Trans. R. Soc. Lond. B Biol. Sci. 278: 245–260, 1977.
 387. Rakic, P., and K. P. Riley. Overproduction and elimination of retinal axons in the fetal rhesus monkey. Science Wash. DC 219: 1441–1444, 1983.
 388. Ramón y Cajal, S. La fine structure des centres nerveux. Proc. R. Soc. Lond. B Biol. Sci. 55: 444–468, 1894.
 389. Ramón y Cajal, S. Histologie du système nerveux de l'homme et des vertébrés. Paris: Maloine, 1911, vol. 2.
 390. Ramos, A., E. L. Schwartz, and E. R. John. Stable and plastic unit discharge patterns during behavioral generalization. Science Wash. DC 192: 393–396, 1976.
 391. Rauschecker, J. P., and W. Singer. Changes in the circuitry of the kitten visual cortex are gated by postsynaptic activity. Nature Lond. 280: 58–60, 1979.
 392. Rauschecker, J. P., and W. Singer. The effects of early visual experience on the cat's visual cortex and their possible explanation by Hebb synapses. J. Physiol. Lond. 310: 215–239, 1981.
 393. Reiff, R., and M. Scheerer. Memory and Hypnotic Age Regression: Developmental Aspects of Cognitive Function Explored Through Hypnosis. New York: International Universities, 1959.
 394. Remy, M. Contribution à l'études de la maladie de Korsakow. Monatsschr. Psychiatr. Neurol. 106: 128–144, 1942.
 395. Ribot, T. Diseases of Memory. New York: Appleton, 1882.
 396. Rigter, H., and H. Van Riezen. Hormones and memory. In: Psychopharmacology: A Generation of Progress, edited by M. A. Lipton, A. Di Mascio, and K. F. Killam. New York: Raven, 1978, p. 677–689.
 397. Riley, A. L., D. A. Zellner, and H. J. F. Duncan. The role of endorphins in animal learning and behavior. Neurosci. Biobehav. Rev. 4: 69–76, 1980.
 398. Rose, F. C., and C. P. Symonds. Persistent memory defect following encephalitis. Brain 83: 195–212, 1960.
 399. Rose, S. P. R. Early visual experience, learning and neurochemical plasticity in the rat and the chick. Philos. Trans. R. Soc. Lond. B Biol. Sci. 278: 307–318, 1977.
 400. Rosene, D. L., and G. Van Hoesen. Hippocampal efferents reach widespread areas of cerebral cortex and amygdala in the rhesus monkey. Science Wash. DC 198: 315–317, 1977.
 401. Rosenkilde, C. E. Functional heterogeneity of the prefrontal cortex in the monkey: a review. Behav. Neural Biol. 25: 301–345, 1979.
 402. Rosenzweig, M. R. Responsiveness of brain size to individual experience. Behavioral and evolutionary implication. In: Development and Evolution of Brain Size: Behavioral Implications, edited by M. E. Hahn, C. Jensen, and B. Dudek. New York: Academic, 1979, p. 263–294.
 403. Rosenzweig, M. R., and E. L. Bennett. Experiential influences on brain anatomy and brain chemistry in rodents. In: Studies on the Development of Behavior and the Nervous System. Early Influences, edited by G. Gottlieb. New York: Academic, 1978, vol. 4, p. 289–327.
 404. Rozin, P. The evolution of intelligence and access to the cognitive unconscious. Prog. Psychobiol. Physiol. Psychol. 6: 245–280, 1976.
 405. Rozin, P. The psychobiological approach to human memory. In: Neural Mechanisms of Learning and Memory, edited by M. R. Rosenzweig and E. L. Bennett. Cambridge, MA: MIT Press, 1976, p. 3–48.
 406. Rubens, A. B. Agnosia. In: Clinical Neuropsychology, edited by K. M. Heilman and E. Valenstein. New York: Oxford Univ. Press, 1979, p. 233–267.
 407. Rumelhart, D., and J. McClelland (editors). Microstructure of Cognition. Cambridge, MA: Bradford, 1986.
 408. Rumelhart, D. E., and D. A. Norman. Representation in memory. In: Steven's Handbook of Experimental Psychology, edited by R. C. Atkinson, R. J. Herrnstein, G. Lindzey, and R. D. Luce. New York: Wiley, in press.
 409. Russell, W. R., and P. W. Nathan. Traumatic amnesia. Brain 69: 280–300, 1946.
 410. Russo, N. J., B. S. Kapp, B. K. Holmquist, and R. E. Musty. Passive avoidance and amydgala lesions: relationship with pituitary‐adrenal system. Physiol. Behav. 16: 191–199, 1976.
 411. Ryle, G. The Concept of Mind. London: Hutchinson, 1949.
 412. Ryugo, D. K., and N. M. Weinberger. Differential plasticity of morphologically distinct neuron populations in the medial geniculate body of the cat during classical conditioning. Behav. Biol. 22: 275–301, 1978.
 413. Sakai, M. Prefrontal unit activity during visually guided lever pressing reaction in the monkey. Brain Res. 81: 297–309, 1974.
 414. Sanders, H. I., and E. K. Warrington. Memory for remote events in amnesic patients. Brain 94: 661–668, 1971.
 415. Saunders, R. C. Impairment in recognition memory after mammillary body lesions in monkeys. Soc. Neurosci. Abstr. 9: 28, 1983.
 416. Scalia, F. The termination of retinal axons in the pretectal region of mammals. J. Comp. Neurol. 145: 223–258, 1972.
 417. Schacter, D. L. Stranger Behind the Engram: Theories of Memory and the Psychology of Science. Hillsdale, NJ: Erlbaum, 1982.
 418. Schacter, D. L. Toward the multidisciplinary study of memory: ontogeny, phylogeny, and pathology of memory systems. In: Neuropsychology of Memory, edited by L. R. Squire and N. Butters. New York: Guilford, 1984, p. 13–23.
 419. Schacter, D. L. Priming of old and new knowledge in amnesic patients. In: Memory Dysfunctions, edited by D. Olton, S. Corkin, and E. Gamzu. New York: NY Acad. Sci., 1985, p. 41–53.
 420. Schacter, D. L. Multiple forms of memory in humans and animals. In: Memory Systems of the Brain: Animal and Human Cognitive Processes, edited by N. Weinberger, G. Lynch, and J. McGaugh. New York: Guilford, 1985, p. 351–379.
 421. Schacter, D. L., and P. Graf. Preserved learning in amnesic patients: perspectives from research on direct priming. J. Clin. Exp. Neuropsychol. In press.
 422. Schacter, D. L., J. L. Harbluk, and D. R. McLachlan. Retrieval without recollection: an experimental analysis of source amnesia. J. Verb. Learn. Verb. Behav. 23: 593–611, 1984.
 423. Schacter, D. L., and M. Moscovitch. Infants, amnesics, and dissociable memory systems. In: Infant Memory, edited by M. Moscovitch. New York: Plenum, 1984, p. 173–216.
 424. Schneiderman, N. Response system divergencies in aversive classical conditioning. In: Classical Conditioning II: Current Research and Theory, edited by A. H. Black and W. F. Prokasy. New York: Appleton‐Century‐Crofts, 1972, p. 341–376.
 425. Schwaber, J. S., B. S. Kapp, G. A. Higgins, and P. R. Rapp. Amygdaloid and basal forebrain direct connections with the nucleus of the solitary tract and the dorsal motor nucleus. J. Neurosci. 2: 1424–1438, 1982.
 426. Scoville, W. B., and B. Milner. Loss of recent memory after bilateral hippocampal lesions. J. Neurol. Psychiatry 20: 11–21, 1957.
 427. Seltzer, B., and D. F. Benson. The temporal pattern of retrograde amnesia in Korsakoff's disease. Neurology 24: 527–530, 1974.
 428. Semon, R. Die Mneme als erhaltendes Prinzip im Wechsel des organischen Geschehens. Leipzig: Engelman, 1904.
 429. Sessions, G. R., G. J. Kant, and G. F. Koob. Locus coeruleus lesions and learning in the rat. Physiol. Behav. 17: 853–859, 1976.
 430. Shallice, T. Specific impairments of planning. Philos. Trans. R. Soc. Lond. B Biol. Sci. 298: 199–209, 1982.
 431. Shatz, C. J., and P. A. Kirkwood. Prenatal development of functional connection in the cat's retinogeniculate pathway. J. Neurosci. 4: 1378–1397, 1984.
 432. Shaw, G. L., E. Harth, and A. B. Scheibel. Cooperativity in brain function: assemblies of approximately 30 neurons. Exp. Neurol. 77: 324–358, 1982.
 433. Shimamura, A., D. Salmon, L. Squire, and N. Butters. Memory dysfunction and word priming in dementia and amnesia. Behav. Neurosci. In press.
 434. Shimamura, A. P., and L. R. Squire. Paired associate learning and priming effects in amnesia: a neuropsychological study. J. Exp. Psychol. Gen. 113: 556–570, 1984.
 435. Shimamura, A. P., and L. R. Squire. Korsakoff's syndrome: the relationship between anterograde amnesia and remote memory impairment. Behav. Neurosci. 100: 165–170, 1986.
 436. Shimamura, A., and L. Squire. A neuropsychological study of fact memory and source amnesia. J. Exp. Psychol. Learn. Mem. Cogn. In press.
 437. Shimamura, A., and L. Squire. Memory and metamemory: A study of the feeling‐of‐knowing phenomenon in amnesic patients. J. Exp. Psychol. Learn. Mem. Cogn. 12: 452–460, 1986.
 438. Sidman, M., L. T. Stoddard, and J. P. Mohr. Some additional quantitative observations of immediate memory in a patient with bilateral hippocampal lesions. Neuropsychologia 6: 245–254, 1968.
 439. Simon, H. A., and W. G. Chase. Skill in chess. Am. Sci. 61: 394–403, 1973.
 440. Singer, W., F. Tretter, and U. Yinon. Evidence for long‐term functional plasticity in the visual cortex of adult cats. J. Physiol. Lond. 324: 239–248, 1982.
 441. Smith, M. L., and B. Milner. Differential effects of frontallobe lesions on cognitive estimation and spatial memory. Neuropsychologia 22: 697–705, 1984.
 442. Smith, O. A., C. A. Astley, J. L. De Vito, J. M. Stein, and K. E. Walsh. Functional analysis of hypothalamic control of the cardiovascular responses accompanying emotional behavior. Federation Proc. 39: 2487–2494, 1980.
 443. Solomon, P. R., and J. W. Moore. Latent inhibition and stimulus generalization of the classically conditioned nictitating membrane response in rabbits (Oryctolagus cuniculus) following dorsal hippocampal ablation. J. Comp. Physiol. Psychol. 89: 1192–1203, 1975.
 444. Speedie, L. J., and K. M. Heilman. Amnestic disturbance following infarction of the left dorsomedial nucleus of the thalamus. Neuropsychologia 20: 597–604, 1982.
 445. Speedie, L. J., and K. M. Heilman. Anterograde memory deficits for visuospatial material after infarction of the right thalamus. Arch. Neurol. 40: 183–186, 1983.
 446. Sperling, G. The information available in brief visual presentations. Psychol. Monogr. Gen. Appl. 74: 1–29, 1960.
 447. Sperry, R. W. Cerebral regulation of motor coordination in monkeys following multiple transection of sensorimotor cortex. J. Neurophysiol. 10: 275–294, 1947.
 448. Sperry, R. W. Physiological plasticity and brain circuit theory. In: Biological and Biochemical Bases of Behavior, edited by H. F. Harlow and C. N. Woolsey. Madison: Univ. Of Wisconsin Press, 1958, p. 401–424.
 449. Sperry, R. W. Preservation of high‐order function in isolated somatic cortex in callosum‐sectioned cat. J. Neurophysiol. 22: 78–87, 1959.
 450. Sperry, R. W. Cerebral organization and behavior. Science Wash. DC 133: 1749–1757, 1961.
 451. Sperry, R. W., and N. Miner. Pattern perception following insertion of mica plates into visual cortex. J. Comp. Physiol. Psychol. 48: 463–469, 1955.
 452. Sperry, R. W., N. Miner, and R. E. Myers. Visual pattern perception following subpial slicing and tantalum wire implantations in the visual cortex. J. Comp. Physiol. Psychol. 48: 50–58, 1955.
 453. Spinelli, D. N., and F. E. Jensen. Plasticity: the mirror of experience. Science Wash. DC 203: 75–78, 1979.
 454. Squire, L. R. Specifying the defect in human amnesia: storage, retrieval, and semantics. Neuropsychologia 18: 368–372, 1980.
 455. Squire, L. R. Two forms of human amnesia: an analysis of forgetting. J. Neurosci. 1: 635–640, 1981.
 456. Squire, L. R. Comparisons between forms of amnesia: some deficits are unique to Korsakoff's syndrome. J. Exp. Psychol. Learn. Mem. Cogn. 8: 560–571, 1982.
 457. Squire, L. R. The neuropsychology of human memory. Annu. Rev. Neurosci. 5: 241–273, 1982.
 458. Squire, L. R. The neuropsychology of memory. In: The Biology of Learning, edited by P. Marler and H. S. Terrace. Berlin: Springer‐Verlag, 1984, p. 667–685. (Dahlem Konferenzen.)
 459. Squire, L. R. Memory and the brain. In: Brain, Cognition, and Education, edited by S. Friedman, K. A. Klivington, and R. W. Peterson. New York: Academic, in press.
 460. Squire, L. R. The neuropsychology of memory dysfunction and its assessment. In: Neuropsychological Assessment of Neuropsychiatric Disorders, edited by I. Grant and K. M. Adams. New York: Oxford Univ. Press, 1986, p. 268–299.
 461. Squire, L. R., and N. Butters (editors). Neuropsychology of Memory. New York: Guilford, 1984.
 462. Squire, L. R., and N. J. Cohen. Human memory and amnesia. In: Neurobiology of Learning and Memory, edited by G. Lynch, J. L. McGaugh, and N. M. Weinberger. New York: Guilford, 1984, p. 3–64.
 463. Squire, L. R., N. J. Cohen, and L. Nadel. The medial temporal region and memory consolidation: a new hypothesis. In: Memory Consolidation: Towards a Psychobiology of Cognition, edited by H. Weingartner and E. Parker. Hillsdale, NJ: Erlbaum, 1984, p. 185–210.
 464. Squire, L. R., N. J. Cohen, and J. A. Zouzounis. Preserved memory in retrograde amnesia: sparing of a recently acquired skill. Neuropsychologia 22: 145–152, 1984.
 465. Squire, L. R., and H. P. Davis. The pharmacology of memory: a neurobiological perspective. Annu. Rev. Pharmacol. Toxicol. 21: 323–356, 1981.
 466. Squire, L. R., and R. Y. Moore. Dorsal thalamic lesions in a noted case of human memory dysfunction. Ann. Neurol. 6: 503–506, 1979.
 467. Squire, L. R., A. Shimamura, and P. Graf. Independence of recognition memory and priming effects: a neuropsychological analysis. J. Exp. Psychol. Learn. Mem. Cogn. 11: 37–44, 1985.
 468. Squire, L. R., A. P. Shimamura, and P. Graf. Strength and duration of priming effects in amnesic patients and normal subjects. Neuropsychologia. In press.
 469. Squire, L. R., P. C. Slater, and P. L. Miller. Retrograde amnesia and bilateral electroconvulsive therapy. Long‐term follow‐up. Arch. Gen. Psychiatry 38: 89–95, 1981.
 470. Squire, L. R., and C. W. Spanis. Long gradient of retrograde amnesia in mice: continuity with the findings in humans. Behav. Neurosci. 98: 345–348, 1984.
 471. Squire, L. R., and S. Zola‐Morgan. The neurology of memory: the case for correspondence between the findings for human and non‐human primate. In: The Physiological Basis of Memory (2nd ed.), edited by J. A. Deutsch. New York: Academic, 1983, p. 200–268.
 472. Squire, L. R., and S. Zola‐Morgan. Neuropsychology of memory: new links between humans and experimental animals. In: Memory Dysfunctions, edited by D. Olton, S. Corkin, and E. Gamzu. New York: NY Acad Sci., 1985, p. 137–149.
 473. Srebro, B., E. C. Azmitia, and J. Winson. Effect of 5‐HT depletion of the hippocampus on neuronal transmission from perforant path through dentate gyrus. Brain Res. 235: 142–147, 1982.
 474. Sretavan, D., and C. J. Shatz. Prenatal development of individual retinogeniculate axons during the period of segregation. Nature Lond. 308: 845–848, 1984.
 475. Stamm, J. S., and S. C. Rosen. Electrical stimulation and steady potential shifts in prefrontal cortex during delayed response performance by monkeys. Acta Biol. Exp. Warsaw 29: 385–399, 1969.
 476. Stamm, J. S., and S. C. Rosen. The locus and crucial time of implication of prefrontal cortex in the delayed response task. In: Psychophysiology of the Frontal Lobes, edited by K. H. Pribram and A. R. Luria. New York: Academic, 1973, p. 139–153.
 477. Steinmetz, J. E., D. G. Lavond, and R. F. Thompson. Classical conditioning of the rabbit eyelid response with mossy fiber stimulation as the conditioned stimulus. Bull. Psychon. Soc. 23: 245–248, 1985.
 478. Stent, G. S. A physiological mechanism for Hebb's postulate of learning. Proc. Natl. Acad. Sci. USA 70: 997–1001, 1973.
 479. Stuss, D. T, E. F. Kaplan, D. F. Benson, W. S. Weir, S. Chiulli, and F. F. Sarazin. Evidence for the involvement of orbitofrontal cortex in memory functions: an interference effect. J. Comp. Physiol. Psychol. 96: 913–925, 1982.
 480. Swanson, L. W., T. J. Teyler, and R. F. Thompson. Hippocampal long‐term potentiation: mechanisms and implications for memory. Neurosci. Res. Program Bull. 20: 613–765, 1982.
 481. Sweet, W. H., G. A. Talland, and F. R. J. Ervin. Loss of recent memory following section of the fornix. Trans. Am. Neurol. Assoc. 84: 876–882, 1959.
 482. Szentagothai, J. The local neuronal apparatus of the cerebral cortex. In: Cerebral Correlates of Conscious Experience, edited by P. A. Buser and A. Rougeul‐Buser. Amsterdam: Elsevier, 1978, p. 131–138.
 483. Talland, G. A. Deranged Memory: A Psychonomic Study of the Amnesic Syndrome. New York: Academic, 1965.
 484. Tanzi, E. I fatti e le induzioni nell'odierna istologia del sistema nervoso. Riv. Sper. Freniatr. Med. Leg. Alienazioni Ment. 19: 419–472, 1893. [Cited in Ramón y Cajal (381b).]
 485. Teuber, H. L. The riddle of frontal lobe function in man. In: The Frontal Granular Cortex and Behavior, edited by J. M. Warren and K. Akert. New York: McGraw‐Hill, 1964, p. 410–477.
 486. Teuber, H. L., B. Milner, and H. C. Vaughan. Persistent anterograde amnesia after stab wound of the basal brain. Neuropsychologia 6: 267–282, 1968.
 487. Teyler, T. J., and P. DiScenna. The hippocampal memory indexing theory. Behav. Neurosci. 100: 147–154, 1986.
 488. Thomas, G. J. Memory: time binding in organisms. In: Neuropsychology of Memory, edited by L. R. Squire and N. Butters. New York: Guilford, 1984, p. 374–384.
 489. Thompson, R. Localization of the “visual memory system” in the white rat. J. Comp. Physiol. Psychol. 69, Suppl. 2: 1–29, 1969.
 490. Thompson, R. Stereotaxic mapping of brainstem areas critical for memory of visual discrimination habits in the rat. Physiol. Psychol. 4: 1–10, 1976.
 491. Thompson, R. A Behavioral Atlas of the Rat Brain. New York: Oxford Univ. Press, 1978.
 492. Thompson, R., and I. Rich. Differential effects of posterior thalamic lesions on retention of various visual habits. J. Comp. Physiol. Psychol. 56: 60–65, 1963.
 493. Thompson, R. F., T. W. Berger, and J. Madden. Cellular processes of learning and memory in the mammalian CNS. Annu. Rev. Neurosci. 6: 447–491, 1983.
 494. Thompson, R. F., L. H. Hicks, and V. B. Shvyrkov (editors). Neural Mechanisms of Goal‐Directed Behavior and Learning. New York: Academic, 1980.
 495. Thompson, R. F., and W. A. Spencer. Habituation: a model phenomenon for a study of neuronal substrates of behavior. Psychol. Rev. 173: 16–43, 1966.
 496. Thorpe, W. H. Learning and Instinct in Animals. Cambridge, MA: Harvard Univ. Press, 1956.
 497. Tischler, M. D., and M. Davis. A visual pathway that mediates fear‐conditioned enhancement of acoustic startle. Brain Res. 276: 55–71, 1983.
 498. Trevarthen, C. B. Double visual learning in split‐brain monkeys. Science Wash. DC 136: 258–259, 1962.
 499. Tsukahara, N. Synaptic plasticity in the mammalian central nervous system. Annu. Rev. Neurosci. 4: 351–379, 1981.
 500. Tsukahara, N., Y. Oda, and T. Notsu. Classical conditioning mediated by the red nucleus in the cat. J. Neurosci. 1: 72–79, 1981.
 501. Tulving, E. Episodic and semantic memory. In: Organization of Memory, edited by E. Tulving and W. Donaldson. New York: Academic, 1972, p. 381–403.
 502. Tulving, E. Elements of Episodic Memory. Oxford, UK: Clarendon, 1983.
 503. Tulving, E. Multiple learning and memory systems. In: Psychology in the 1990s, edited by K. Lagerspetz and P. Niemi. Amsterdam: Elsevier/North‐Holland, 1984, p. 163–184.
 504. Turner, A. M., and W. T. Greenough. Differential rearing effects on rat visual cortex synapses. I. Synaptic and neuronal density and synapses per neuron. Brain. Res. 329: 195–203, 1985.
 505. Udin, S. B. Abnormal visual input leads to development of abnormal axon trajectories in frogs. Nature Lond. 301: 336–338, 1983.
 506. Udin, S. B., and M. J. Keating. Plasticity in a central nervous pathway in Xenopus: anatomical changes in the isthmotectal projection after larval eye rotation. J. Comp. Neurol. 203: 575–594, 1981.
 507. Ungerleider, L. G., and R. Desimone. Cortical connections of visual area MT in the macaque. J. Comp. Neurol. 248: 190–222, 1986.
 508. Ungerleider, W., and M. Mishkin. Two cortical visual systems. In: The Analysis of Visual Behavior, edited by D. J. Ingel, R. J. W. Mansfield, and M. A. Goodale. Cambridge, MA: MIT Press, 1982, p. 549–586.
 509. Van Heerden, P. J. A new method of storing and retrieving information. Appl. Opt. 2: 387–392, 1963.
 510. Van Heerden, P. J. The Foundation of Empirical Knowledge, With a Theory of Artificial Intelligence. Wassenaar, The Netherlands: Wistik, 1968.
 511. Van Hoesen, G. W. The parahippocampal gyrus. Trends Neurosci. 5: 345–350, 1982.
 512. Van Hoesen, G. W., D. N. Pandya, and N. Butters. Cortical afferents to the entorhinal cortex of the rhesus monkey. Science Wash. DC 175: 1471–1473, 1972.
 513. Van Hoesen, G. W., D. N. Pandya, and N. Butters. Some connections of the entorhinal (area 28) and perirhinal (area 35) cortices of the rhesus monkey. II. Frontal lobe afferents. Brain Res. 95: 25–38, 1975.
 514. Van Wimersma Greidanus, T. J. B., G. Croiset, E. Bakker, and H. Bouman. Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH/4–10) on avoidance behavior. Physiol. Behav. 22: 291–295, 1979.
 515. Victor, M., R. D. Adams, and G. H. Collins. The Wernicke‐Korsakoff Syndrome. Philadelphia, PA: Davis, 1971.
 516. Vincent, S. R, T. Hökfelt, L. R. Skirboll, and J. Y. Wu. Hypothalamic gamma‐aminobutyric acid neurons project to the neocortex. Science Wash. DC 220: 1309–1311, 1983.
 517. Volpe, B. T., and W. Hirst. Amnesia following the rupture and repair of an anterior communicating artery aneurysm. J. Neurol. Neurosurg. Psychiatry 46: 704–709, 1983.
 518. Volpe, B. T., and W. Hirst. The characterization of an amnesic syndrome following hypoxic ischemic injury. Arch. Neurol. 40: 436–445, 1983.
 519. Von Bonin, G., and P. Bailey. The Neocortex of Macaca mulatta. Urbana: Univ. of Illinois Press, 1947.
 520. Walker, A. E. A cytoarchitectural study of the prefrontal area of the macaque monkey. J. Comp. Neurol. 73: 59–86, 1940.
 521. Walters, E. T., and J. M. Byrne. Associative conditioning of single sensory neurons suggests a cellular mechanism for learning. Science Wash. DC 219: 405–408, 1983.
 522. Warrington, E. K., and L. Weiskrantz. A new method of testing long‐term retention with special reference to amnesic patients. Nature Lond. 217: 972–974, 1968.
 523. Warrington, E. K., and L. Weiskrantz. The amnesic syndrome: consolidation or retrieval? Nature Lond. 228: 628–630, 1970.
 524. Warrington, E. K., and L. Weiskrantz. The effect of prior learning on subsequent retention in amnesic patients. Neuropsychologia 12: 419–428, 1974.
 525. Warrington, E. K., and L. Weiskrantz. Amnesia: a disconnection syndrome? Neuropsychologia 20: 233–248, 1982.
 526. Waugh, N. C., and D. A. Norman. Primary memory. Psychol. Rev. 72: 89–104, 1965.
 527. Weinberger, N. M. Effects of conditioned arousal on the auditory system. In: The Neural Basis of Behavior, edited by A. L. Beckman. New York: Spectrum, 1982, p. 63–91.
 528. Weinberger, N. M., D. M. Diamond, and T. M. McKenna. Initial events in conditioning: plasticity in the pupillomotor and auditory systems. In: Neurobiology of Learning and Memory, edited by G. Lynch, J. L. McGaugh, and N. M. Weinberger. New York: Guilford, 1984, p. 197–227.
 529. Weiskrantz, L. Comparative aspects of studies in amnesia. Philos. Trans. R. Soc. Lond. B Biol. Sci. 298: 97–109, 1982.
 530. Weiskrantz, L., and E. K. Warrington. Conditioning in amnesic patients. Neuropsychologia 17: 187–194, 1979.
 531. Wenk, H., V. Bigl, and U. Meyer. Cholinergic projections from magnocellular nuclei of the basal forebrain to cortical areas in rats. Brain Res. Rev. 2: 295–316, 1980.
 532. Werka, T., J. Skar, and H. Ursin. Exploration and avoidance in rats with lesions in amygdala and piriform cortex. J. Comp. Physiol. Psychol. 92: 672–681, 1978.
 533. Whitehouse, P. J., D. L. Price, R. G. Struble, A. W. Clark, J. T. Coyle, and M. R. De Long. Alzheimer's disease and senile dementia; loss of neurons in the basal forebrain. Science Wash. DC 215: 1237–1239, 1982.
 534. Wickelgren, W. A. Sparing of short‐term memory in an amnesic patient: implications for a strength theory of memory. Neuropsychologia 6: 235–244, 1968.
 535. Wickelgren, W. A. Chunking and consolidation: a theoretical synthesis of semantic networks, configuring in conditioning, S‐R vs. cognitive learning, normal forgetting, the amnesic syndrome and the hippocampal arousal system. Psychol. Rev. 86: 44–60, 1979.
 536. Wiesel, T. N. Postnatal development of the visual cortex and the influence of environment. Nature Lond. 299: 583–591, 1982.
 537. Wiesel, T. N., and D. H. Hubel. Single‐cell responses in striate cortex of kittens deprived of vision in one eye. J. Neurophysiol. 26: 1003–1017, 1963.
 538. Wiesel, T. N., and D. H. Hubel. Comparison of the effects of unilateral and bilateral eye closure on cortical unit responses in kittens. J. Neurophysiol. 28: 1029–1040, 1965.
 539. Williams, M., and J. Pennybacker. Memory disturbances in third ventricle tumours. J. Neurol. Neurosurg. Psychiatry 17: 115–123, 1954.
 540. Winocur, G., S. Oxbury, R. Roberts, V. Agnetti, and C. Davis. Amnesia in a patient with bilateral lesions to the thalamus. Neuropsychologia 22: 123–143, 1984.
 541. Winograd, T. Frame representations and the declarativeprocedural controversy. In: Representation and Understanding: Studies in Cognitive Science, edited by D. Bobrow and A. Collins. New York: Academic, 1975, p. 185–210.
 542. Winson, J. Influence of raphe nuclei on neuronal transmission from perforant pathway through dentate gyrus. J. Neurophysiol. 44: 937–950, 1980.
 543. Winson, J., and C. Abzug. Neuronal transmission through hippocampal pathways dependent on behavior. J. Neurophysiol. 41: 716–732, 1978.
 544. Winston, P. H. Artificial Intelligence. Menlo Park, CA: Addison‐Wesley, 1977.
 545. Wood, F., V. Ebert, and M. Kinsbourne. The episodicsemantic memory distinction in memory and amnesia: clinical and experimental observations. In: Human Memory and Amnesia, edited by L. Cermak. Hillsdale, NJ: Erlbaum, 1982, p. 167–194.
 546. Woody, C. D. (editor). Conditioning: Representation of Involved Neural Functions. New York: Plenum, 1982, p. 233–248.
 547. Woody, C. D. Memory, Learning, and Higher Function: A Cellular View. New York: Springer‐Verlag, 1982.
 548. Yeo, C. H., M. J. Hardiman, and M. Glickstein. Discrete lesions of the cerebellar cortex abolish the classically conditioned nictitating membrane response of the rabbit. Behav. Brain Res. 13: 261–266, 1984.
 549. Yeo, C. H., M. J. Hardiman, M. Glickstein, and I. S. Russell. Lesions of cerebellar nuclei abolish the classically conditioned nictitating membrane response. Soc. Neurosci. Abstr. 8: 22, 1982.
 550. Yin, R. K. Face recognition by brain‐injured patients: a dissociable ability? Neuropsychologia 8: 395–402, 1970.
 551. Young, J. Z. Learning as a process of selection and amplification. J. R. Soc. Med. 72: 801–814, 1979.
 552. Zangwill, O. L. The cerebral localisation of psychological function. Adv. Sci. 20: 335–344, 1963.
 553. Zeki, S. M. Uniformity and diversity of structure and function in rhesus monkey prestriate visual cortex. J. Physiol. Lond. 277: 273–290, 1978.
 554. Zigmond, M. J., A. L. Acheson, L. A. Chiodo, and E. M. Stricker. Increased norepinephrine turnover and increased firing rate in residual neurons after NE‐depleting lesions. Soc. Neurosci. Abstr. 7: 456, 1981.
 555. Zola‐Morgan, S., N. J. Cohen, and L. R. Squire. Recall of remote episodic memory in amnesia. Neuropsychologia 21: 487–500, 1983.
 556. Zola‐Morgan, S., and L. R. Squire. Preserved learning in monkeys with medial temporal lesions: sparing of motor and cognitive skills. J. Neurosci. 4: 1072–1085, 1984.
 557. Zola‐Morgan, S., and L. R. Squire. Amnesia in monkeys following lesions of the mediodorsal nucleus of the thalamus. Ann. Neurol. 17: 558–564, 1985.
 558. Zola‐Morgan, S., and L. R. Squire. Medial temporal lesions in monkeys impair memory in a variety of tasks sensitive to amnesia. Behav. Neurosci. 99: 22–34, 1985.
 559. Zola‐Morgan, S., and L. R. Squire. Memory impairment in monkeys following lesions of the hippocampus. Behav. Neurosci. 100: 155–160, 1986.
 560. Zola‐Morgan, S., and L. R. Squire. Complementary approaches to the study of memory: human amnesia and animal models. In: Memory Systems of the Brain: Animal and Human Cognitive Processes, edited by N. Weinberger, J. McGaugh, and G. Lynch. New York: Guilford, 1985, p. 463–477.
 561. Zola‐Morgan, S., L. R. Squire, and D. Amaral. Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to the CA1 field of the hippocampus. J. Neurosci. In press.
 562. Zola‐Morgan. S., L. R. Squire, and M. Mishkin. The neuroanatomy of amnesia: amygdala‐hippocampus versus temporal stem. Science Wash. DC 218: 1337–1339, 1982.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

How to Cite

Larry R. Squire. Memory: Neural Organization and Behavior. Compr Physiol 2011, Supplement 5: Handbook of Physiology, The Nervous System, Higher Functions of the Brain: 295-371. First published in print 1987. doi: 10.1002/cphy.cp010508