Comprehensive Physiology Wiley Online Library

Structural and Metabolic Processes Directly Related to Action Potential Propagation

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Structure
1.1 Optical Properties
1.2 Heat Production
2 Recovery Processes Following Impulse Conduction
2.1 Properties of the Sodium‐Potassium Pump
2.2 Recovery Heat
2.3 Oxygen Consumption
2.4 Intrinsic Fluorescence
2.5 Metabolic Intermediates
2.6 Metabolic Control
2.7 Electrical Phenomena Accompanying Recovery
3 Prognosis
Figure 1. Figure 1.

Fluorescence increase (noisy trace) of a merocyanine dye [dye I of ] during the action potential (thin trace) in a giant axon from Loligo pealei. The fluorescence increase has the same time course as the potential change, and thus this fluorescence change appears to be related to membrane potential and not to ionic current or membrane permeability. The dye merocyanine I is‐5‐[(3‐sulfopropyl‐2‐(3H)‐benzoxazolydine)‐2‐butenyli‐dene]‐1,3‐dibutyl‐2‐thiobarbituric acid. In this and other such figures the direction of the arrow to the right of the trace indicates the direction of an increase in intensity, and the length of the arrow corresponds to the stated value of the change in intensity divided by the resting intensity for a single sweep. Temperature, 15° C; 16 sweeps averaged.

From Cohen et al.
Figure 2. Figure 2.

Merocyanine I fluorescence changes (top trace) during voltage‐clamp steps (middle trace) in a giant axon from L. pealei. The current density is shown in the bottom trace. The fluorescence changes have a time course similar to that of the potential. Electrical compensation for the resistance in series with the membrane was used [see and for effects of compensation on optical records]. Hyperpolarizing is downward; inward current is downward. Temperature, 13° C; 25 sweeps averaged.

From Cohen et al.
Figure 3. Figure 3.

Merocyanine I fluorescence change versus membrane potential in squid axon. The fluorescence is linearly related to membrane potential. The origin of the potential scale is the resting potential.

From Cohen et al.
Figure 4. Figure 4.

Change in intensity (retardation) versus membrane potential in a squid axon. Experimental points fell near the curve, which represents potential squared with an origin at + 125 mV. The origin of the potential scale is the resting potential. Voltage steps of 0.3‐ms duration were used. Hyperpol., hyperpolarization; depol., depolarization.

From Cohen et al.
Figure 5. Figure 5.

The 90° light‐scattering change (irregular line) measured in L. forbesi during the action potential (regular line). The light‐scattering change had two phases: an early increase that accompanied the spike and a slow, long‐lasting increase that continued long after the action potential. Temperature, 12° C; 8 × 103 sweeps averaged.

From Cohen et al.
Figure 6. Figure 6.

The 90° light‐scattering change (top line) in L. forbesi during voltage‐clamp potential steps (middle line). Current densities are shown in bottom line. There was a large scattering change during depolarizing step but only a small change during hyperpolarizing step. Temperature, 19° C; 9 × 102 sweeps averaged.

From Cohen et al.
Figure 7. Figure 7.

Changes in 90° light scattering (heavy lines) in L. pealei resulting from two different depolarizing steps (bottom line). A 50‐mV step (solid curve, bottom trace) led to a large increase in permeability and a large inward current (solid curve, middle trace). A large scattering increase resulted. The potential reached by 92‐mV depolarizing step (dashed curve, bottom trace) was near equilibrium potential, and thus the current (dashed curve, middle trace) was much smaller even though the permeability increase was still large. When the current was blocked, there was no clearly demonstrable scattering change. This axon had been microinjected with tetraethylammonium bromide, final concentration 24 mM, to block delayed outward currents. Temperature, 12° C; 2.4 × 102 sweeps averaged.

From Cohen et al.
Figure 8. Figure 8.

Effect of replacing a chloride seawater with isethionate‐glutamate seawater on the 90° light scattering in L. pealei. Scattering change was reduced in size in the isethionate‐glutamate seawater. The current resulted from a 120‐mV depolarizing potential step. Temperature, 12° C; 64 sweeps averaged.

From Cohen et al.
Figure 9. Figure 9.

Changes in temperature of the nonmyelinated fibers of a rabbit vagus nerve following individual stimulations applied at the arrow. Temperature, 5.3° C; 102 sweeps averaged.

From Howarth et al.
Figure 10. Figure 10.

Relation between [ATP]i and Na efflux in dialyzed squid axons (double logarithmic plot). Horizontal bar indicates the range of [ATP] found in fresh axons. Inset shows data for 0–200 μM ATP plotted on a linear scale. All data normalized to 15° C.

From Brinley & Mullins
Figure 11. Figure 11.

Relation between [Na]i and Na+ efflux in dialyzed squid axons. Dialysis solutions contained 5 mM ATP and 5 mM phosphoarginine. Internal Na+ was substituted for K+, their combined concentration being kept at 380 mM. Artificial seawater contained Na+, 430 mM; K+, 9 mM; Ca2+, 9 mM; Mg2+, 48 mM; Cl, 496 mM. The different symbols represent different axons.

From Brinley & Mullins
Figure 12. Figure 12.

Effects of [K]o and [Na]o on ouabain‐sensitive sodium efflux from intact squid axons. Efflux is expressed relative to that into artificial seawater (ASW) containing 460 mM NaCl and 10 mM KCl. External sodium was replaced with choline (□, ) or dextrose (▪, ).

From Baker et al.
Figure 13. Figure 13.

Relation between [K]o and ATP‐dependent K+ influx in dialyzed squid axons. Each point is a comparison between 10 mM K and the test [K]o. For seawater (SW) composition, see Fig. . Dialysis fluid contained Na+, 80 mM; and K+, 310 mM.

From Mullins & Brinley
Figure 14. Figure 14.

Relation between [Na]i and ATP‐dependent K+ influx in dialyzed squid axons. The points are comparisons between [Na]i = 80 mM and the test [Na]i. For internal and external fluid composition, see Fig. .

From Mullins & Brinley
Figure 15. Figure 15.

Transport coupling ratio in squid giant axon. Upper graph, the dependence of the ratio of ATP‐dependent Na+ efflux to ATP‐dependent K+ influx on internal sodium concentration. Lower graph, the ratio of Na to K coupling as a function of [ATP]i

Slightly modified from Mullins & Brinley
Figure 16. Figure 16.

Total heat production (initial heat plus recovery heat) in rabbit desheathed vagal nonmyelinated nerves at 21°C after 20 shocks at 2.5 Hz (short horizontal bar). The records labeled N were taken in ordinary Locke's solution. Alternating with these are the responses obtained after the nerve had been equilibrated in: a K‐free Locke's solution, a solution in which all Na+ had been replaced by K+ (KCl), and a Locke's solution containing 1 mM ouabain. KCl record shows the heating effect of the stimulating current. The fact that nominally K‐free solutions do not abolish poststimulus heat production (or oxygen consumption or membrane hyperpolarization) is explained by assuming that enough K+ leaks out of the cell to activate the sodium pump. The slight increase in delayed heat production may be due to a greater entry of Na+ during spike conduction in K‐free media.

From Howarth et al.
Figure 17. Figure 17.

Changes in the rate of respiration of a crab nerve during and after a tetanus. The nerve was bathed in seawater containing 10 mM K+. Stimulation started at the arrow and lasted for 6 min at 2 Hz (A); or for 10 min at 4 Hz (B); or for 10 min at 4 Hz, then 8 min at 10 Hz (C). Temperature, 16° C.

From Baker & Connelly
Figure 18. Figure 18.

Effect of ouabain on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 35° C. Arrows indicate the 5‐s period of stimulation at 30 Hz. Upper trace, control in normal Locke's solution; lower trace, after a 10‐min exposure to ouabain (1 mM).

From Landowne & Ritchie
Figure 19. Figure 19.

Effect of lithium and of calcium on the intrinsic fluorescence response to stimulation of rabbit cervical vagus nerve at 31°C. Arrows indicate the 5‐s period of stimulation at 30 Hz. a, control in normal Locke's solution; b, after soaking in a lithium‐substituted Locke's solution; c, after soaking in a lithium‐Locke's solution containing no calcium.

From Landowne & Ritchie
Figure 20. Figure 20.

Effect of ouabain on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 20° C. Between the arrows the nerve was stimulated for 15 s at 37 Hz. a, in normal Locke's solution; b, in the presence of ouabain (1 mM). Note disappearance of a slow component in the presence of ouabain.

From Landowne & Ritchie
Figure 21. Figure 21.

Effect of calcium on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 22° C. Arrows indicate a 5‐s period of stimulation at 37 Hz. a, in normal Locke's solution; b, after 15‐min exposure to Ca‐free Locke's solution.

From Landowne & Ritchie
Figure 22. Figure 22.

Concentrations (μmol/g wet wt) of ATP (•), ADP (), AMP (⊙), phosphocreatine (⊕), and Pi (○) at rest and after 15‐s period of stimulation at 50 Hz in desheathed rabbit vagus nerves at 37° C. Stimulation was between −15 and 0 s.

From Chmouliovsky et al.
Figure 23. Figure 23.

Glycogen breakdown and glycolytic (Embden‐Meyerhof) pathway.

Figure 24. Figure 24.

Effect of ouabain on the posttetanic hyperpolarization of the nonmyelinated fibers of rabbit vagus nerves. Stimulation was at 370 Hz for 5 s. a, control posttetanic hyperpolarizing response; b, response when 1 mM ouabain was added 30 s after end of stimulation; c, response after 12 min in ouabain. In order to reduce shunting of the pump current by Cl, all chloride in the Locke's solution was replaced with isethionate.

From Rang & Ritchie


Figure 1.

Fluorescence increase (noisy trace) of a merocyanine dye [dye I of ] during the action potential (thin trace) in a giant axon from Loligo pealei. The fluorescence increase has the same time course as the potential change, and thus this fluorescence change appears to be related to membrane potential and not to ionic current or membrane permeability. The dye merocyanine I is‐5‐[(3‐sulfopropyl‐2‐(3H)‐benzoxazolydine)‐2‐butenyli‐dene]‐1,3‐dibutyl‐2‐thiobarbituric acid. In this and other such figures the direction of the arrow to the right of the trace indicates the direction of an increase in intensity, and the length of the arrow corresponds to the stated value of the change in intensity divided by the resting intensity for a single sweep. Temperature, 15° C; 16 sweeps averaged.

From Cohen et al.


Figure 2.

Merocyanine I fluorescence changes (top trace) during voltage‐clamp steps (middle trace) in a giant axon from L. pealei. The current density is shown in the bottom trace. The fluorescence changes have a time course similar to that of the potential. Electrical compensation for the resistance in series with the membrane was used [see and for effects of compensation on optical records]. Hyperpolarizing is downward; inward current is downward. Temperature, 13° C; 25 sweeps averaged.

From Cohen et al.


Figure 3.

Merocyanine I fluorescence change versus membrane potential in squid axon. The fluorescence is linearly related to membrane potential. The origin of the potential scale is the resting potential.

From Cohen et al.


Figure 4.

Change in intensity (retardation) versus membrane potential in a squid axon. Experimental points fell near the curve, which represents potential squared with an origin at + 125 mV. The origin of the potential scale is the resting potential. Voltage steps of 0.3‐ms duration were used. Hyperpol., hyperpolarization; depol., depolarization.

From Cohen et al.


Figure 5.

The 90° light‐scattering change (irregular line) measured in L. forbesi during the action potential (regular line). The light‐scattering change had two phases: an early increase that accompanied the spike and a slow, long‐lasting increase that continued long after the action potential. Temperature, 12° C; 8 × 103 sweeps averaged.

From Cohen et al.


Figure 6.

The 90° light‐scattering change (top line) in L. forbesi during voltage‐clamp potential steps (middle line). Current densities are shown in bottom line. There was a large scattering change during depolarizing step but only a small change during hyperpolarizing step. Temperature, 19° C; 9 × 102 sweeps averaged.

From Cohen et al.


Figure 7.

Changes in 90° light scattering (heavy lines) in L. pealei resulting from two different depolarizing steps (bottom line). A 50‐mV step (solid curve, bottom trace) led to a large increase in permeability and a large inward current (solid curve, middle trace). A large scattering increase resulted. The potential reached by 92‐mV depolarizing step (dashed curve, bottom trace) was near equilibrium potential, and thus the current (dashed curve, middle trace) was much smaller even though the permeability increase was still large. When the current was blocked, there was no clearly demonstrable scattering change. This axon had been microinjected with tetraethylammonium bromide, final concentration 24 mM, to block delayed outward currents. Temperature, 12° C; 2.4 × 102 sweeps averaged.

From Cohen et al.


Figure 8.

Effect of replacing a chloride seawater with isethionate‐glutamate seawater on the 90° light scattering in L. pealei. Scattering change was reduced in size in the isethionate‐glutamate seawater. The current resulted from a 120‐mV depolarizing potential step. Temperature, 12° C; 64 sweeps averaged.

From Cohen et al.


Figure 9.

Changes in temperature of the nonmyelinated fibers of a rabbit vagus nerve following individual stimulations applied at the arrow. Temperature, 5.3° C; 102 sweeps averaged.

From Howarth et al.


Figure 10.

Relation between [ATP]i and Na efflux in dialyzed squid axons (double logarithmic plot). Horizontal bar indicates the range of [ATP] found in fresh axons. Inset shows data for 0–200 μM ATP plotted on a linear scale. All data normalized to 15° C.

From Brinley & Mullins


Figure 11.

Relation between [Na]i and Na+ efflux in dialyzed squid axons. Dialysis solutions contained 5 mM ATP and 5 mM phosphoarginine. Internal Na+ was substituted for K+, their combined concentration being kept at 380 mM. Artificial seawater contained Na+, 430 mM; K+, 9 mM; Ca2+, 9 mM; Mg2+, 48 mM; Cl, 496 mM. The different symbols represent different axons.

From Brinley & Mullins


Figure 12.

Effects of [K]o and [Na]o on ouabain‐sensitive sodium efflux from intact squid axons. Efflux is expressed relative to that into artificial seawater (ASW) containing 460 mM NaCl and 10 mM KCl. External sodium was replaced with choline (□, ) or dextrose (▪, ).

From Baker et al.


Figure 13.

Relation between [K]o and ATP‐dependent K+ influx in dialyzed squid axons. Each point is a comparison between 10 mM K and the test [K]o. For seawater (SW) composition, see Fig. . Dialysis fluid contained Na+, 80 mM; and K+, 310 mM.

From Mullins & Brinley


Figure 14.

Relation between [Na]i and ATP‐dependent K+ influx in dialyzed squid axons. The points are comparisons between [Na]i = 80 mM and the test [Na]i. For internal and external fluid composition, see Fig. .

From Mullins & Brinley


Figure 15.

Transport coupling ratio in squid giant axon. Upper graph, the dependence of the ratio of ATP‐dependent Na+ efflux to ATP‐dependent K+ influx on internal sodium concentration. Lower graph, the ratio of Na to K coupling as a function of [ATP]i

Slightly modified from Mullins & Brinley


Figure 16.

Total heat production (initial heat plus recovery heat) in rabbit desheathed vagal nonmyelinated nerves at 21°C after 20 shocks at 2.5 Hz (short horizontal bar). The records labeled N were taken in ordinary Locke's solution. Alternating with these are the responses obtained after the nerve had been equilibrated in: a K‐free Locke's solution, a solution in which all Na+ had been replaced by K+ (KCl), and a Locke's solution containing 1 mM ouabain. KCl record shows the heating effect of the stimulating current. The fact that nominally K‐free solutions do not abolish poststimulus heat production (or oxygen consumption or membrane hyperpolarization) is explained by assuming that enough K+ leaks out of the cell to activate the sodium pump. The slight increase in delayed heat production may be due to a greater entry of Na+ during spike conduction in K‐free media.

From Howarth et al.


Figure 17.

Changes in the rate of respiration of a crab nerve during and after a tetanus. The nerve was bathed in seawater containing 10 mM K+. Stimulation started at the arrow and lasted for 6 min at 2 Hz (A); or for 10 min at 4 Hz (B); or for 10 min at 4 Hz, then 8 min at 10 Hz (C). Temperature, 16° C.

From Baker & Connelly


Figure 18.

Effect of ouabain on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 35° C. Arrows indicate the 5‐s period of stimulation at 30 Hz. Upper trace, control in normal Locke's solution; lower trace, after a 10‐min exposure to ouabain (1 mM).

From Landowne & Ritchie


Figure 19.

Effect of lithium and of calcium on the intrinsic fluorescence response to stimulation of rabbit cervical vagus nerve at 31°C. Arrows indicate the 5‐s period of stimulation at 30 Hz. a, control in normal Locke's solution; b, after soaking in a lithium‐substituted Locke's solution; c, after soaking in a lithium‐Locke's solution containing no calcium.

From Landowne & Ritchie


Figure 20.

Effect of ouabain on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 20° C. Between the arrows the nerve was stimulated for 15 s at 37 Hz. a, in normal Locke's solution; b, in the presence of ouabain (1 mM). Note disappearance of a slow component in the presence of ouabain.

From Landowne & Ritchie


Figure 21.

Effect of calcium on the intrinsic fluorescence response to stimulation of a rabbit cervical vagus nerve at 22° C. Arrows indicate a 5‐s period of stimulation at 37 Hz. a, in normal Locke's solution; b, after 15‐min exposure to Ca‐free Locke's solution.

From Landowne & Ritchie


Figure 22.

Concentrations (μmol/g wet wt) of ATP (•), ADP (), AMP (⊙), phosphocreatine (⊕), and Pi (○) at rest and after 15‐s period of stimulation at 50 Hz in desheathed rabbit vagus nerves at 37° C. Stimulation was between −15 and 0 s.

From Chmouliovsky et al.


Figure 23.

Glycogen breakdown and glycolytic (Embden‐Meyerhof) pathway.



Figure 24.

Effect of ouabain on the posttetanic hyperpolarization of the nonmyelinated fibers of rabbit vagus nerves. Stimulation was at 370 Hz for 5 s. a, control posttetanic hyperpolarizing response; b, response when 1 mM ouabain was added 30 s after end of stimulation; c, response after 12 min in ouabain. In order to reduce shunting of the pump current by Cl, all chloride in the Locke's solution was replaced with isethionate.

From Rang & Ritchie
References
 1. Abbott, B. C., A. V. Hill, and J. V. Howarth. The positive and negative heat production associated with a single impulse. Proc. Roy. Soc. London. Ser. B 148: 149–187, 1958.
 2. Abbott, B. C., and J. V. Howarth. Heat studies in excitable tissues. Physiol. Rev. 53: 120–158, 1973.
 3. Albers, R. W. Biochemical aspects of active transport. Ann. Rev. Biochem. 36: 727–756, 1967.
 4. Aubert, X., B. Chance, and R. D. Keynes. Optical studies of biochemical events in the electric organ of Electrophorus. Proc. Roy. Soc. Lond. Ser. B 160: 211–245, 1964.
 5. Baker, P. F. Phosphorus metabolism of intact crab nerve and its relation to the active transport of ions. J. Physiol. London 180: 383–423, 1965.
 6. Baker, P. F. Transport and metabolism of calcium ions in nerve. Progr. Biophys. Mol. Biol. 24: 117–223, 1972.
 7. Baker, P. F., M. P. Blaustein, R. D. Keynes, J. Manil, T. I. Shaw, and R. A. Steinhardt. The ouabain‐sensitive fluxes of sodium and potassium in squid giant axons. J. Physiol. London 200: 459–496, 1969.
 8. Baker, P. F., and C. M. Connelly. Some properties of the external activation site of the sodium pump in crab nerve. J. Physiol. London 185: 270–297, 1966.
 9. Baker, P. F., and A. C. Crawford. Mobility and transport of magnesium in squid giant axons. J. Physiol. London 227: 855–874, 1972.
 10. Baker, P. F., and T. I. Shaw. A comparison of the phosphorus metabolism of intact squid nerve with that of the isolated axoplasm and sheath. J. Physiol. London 180: 424–438, 1965.
 11. Baker, P. F., and J. S. Willis. On the number of sodium pumping sites in cell membranes. Biochim. Biophys. Acta 183: 646–649, 1969.
 12. Baker, P. F., and J. S. Willis. Inhibition of the sodium pump in squid axons by cardiac glycosides: dependence on extracellular ions and metabolism. J. Physiol. London 224: 463–476, 1972.
 13. Barry, P. H., and A. B. Hope. Electroosmosis in membranes: effects of unstirred layers and transport numbers. I. Theory. Biophys. J. 9: 700–728, 1969.
 14. Baylor, D. A., and J. G. Nicholls. After‐effects of nerve impulses on signalling in the central nervous system of the leech. J. Physiol. London 203: 571–589, 1969.
 15. Bennett, H. S. The microscopical investigation of biological materials with polarized light. In: McClung's Handbook of Microscopical Techniques (3rd ed.), edited by R. M. Jones. New York: Hoeber, 1950, p. 591–677.
 16. Berestovsky, G. N., G. M. Frank, E. A. Liberman, V. Z. Lunevsky, and V. D. Razhin. Electrooptical phenomena in bimolecular phospholipid membranes. Biochim. Biophys. Acta 219: 263–275, 1970.
 17. Berestovsky, G. N., V. Z. Lunevsky, V. D. Razhin, and V. S. Musienko. Rapid changes in birefringence of the nerve fiber membrane during excitation. Dokl. Akad. Nauk. SSSR 189: 203–206, 1969.
 18. Blaustein, M. P. The interrelationship between sodium and calcium fluxes across cell membranes. Rev. Physiol. Biochem. Pharmacol. 70: 33–82, 1974.
 19. Brand, L., and J. R. Gohlke. Fluorescent probes for structure. Ann. Rev. Biochem. 41: 843–868, 1972.
 20. Brandt, P. W., A. R. Freeman, J. P. Reuben, and H. Grundfest. Variations in spacing between axon and Schwann membranes induced in lobster nerve fibers by currents and fluxes. Biol. Bull. 129: 400, 1965.
 21. Brinley, F. J., Jr. Sodium, potassium, and chloride concentrations and fluxes in the isolated giant axon of Homarus. J. Neurophysiol. 28: 742–772, 1965.
 22. Brinley, F. J., Jr., and L. J. Mullins. Sodium fluxes in internally dialyzed squid axons. J. Gen. Physiol. 52: 181–211, 1968.
 23. Brodwick, M. S., and D. Junge. Post‐stimulus hyperpolarization and slow potassium conductance increase in increase in Aplysia giant neurone. J. Physiol. London 223: 549–570, 1972.
 24. Brostrom, C. O., F. L. Hunkeler, and E. G. Krebs. The regulation of skeletal muscle phosphorylase kinase by Ca2+. J. Biol. Chem. 246: 1961–1967, 1971.
 25. Buytendijk, F. J. J. Over het zuurstof‐verbruik van het zenuwstesel. Koninkl. Ned. Akad. Wetenschap. Verslag. Gewone Vergader. Afdel. Nat. 19: 615–621, 1910.
 26. Caldwell, P. C., A. L. Hodgkin, R. D. Keynes, and T. I. Shaw. The effect of injecting “energy rich” phosphate compounds on the active transport of ions in the giant axons of Loligo. J. Physiol. London 152: 561–590, 1960.
 27. Carbone, E., H. Sato, M. Hallett, and I. Tasaki. Structural studies of the squid giant axon using birefringence techniques (Abstract). Biophys. Soc. Meeting, 17th, Columbus, Ohio, 1973, p. 241a.
 28. Carnay, L. D., and W. H. Barry. Turbidity, birefringence and fluorescence changes in skeletal muscle coincident with the action potential. Science 165: 608–609, 1969.
 29. Chance, B., and F. Jobsis. Changes in fluorescence in a frog sartorius muscle following a twitch. Nature 184: 195–196, 1959.
 30. Chandler, W. K., A. L. Hodgkin, and H. Meves. The effect of changing the internal solution on sodium inactivation and related phenomena in giant axons. J. Physiol. London 180: 821–836, 1965.
 31. Chmouliovsky, M., M. Schorderet, and R. W. Straub. Effect of electrical activity on the concentration of phosphorylated metabolites and inorganic phosphate in mammalian nonmyelinated nerve fibres. J. Physiol. London 202: 90p–92p, 1969.
 32. Cohen, L. B. Changes in neuron structure during action potential propagation and synaptic transmission. Physiol. Rev. 53: 373–418, 1973.
 33. Cohen, L. B., B. Hille, and R. D. Keynes. Light scattering and birefringence changes during activity in the electric organ of Electrophorus electricus. J. Physiol. London 203: 489–509, 1969.
 34. Cohen, L. B., B. Hille, and R. D. Keynes. Changes in axon birefringenece during the action potential. J. Physiol. London 211: 495–515, 1970.
 35. Cohen, L. B., B. Hille, R. D. Keynes, D. Landowne, and E. Rojas. Analysis of the potential‐dependent changes in optical retardation in the squid giant axon. J. Physiol. London 218: 205–237, 1971.
 36. Cohen, L. B., R. D. Keynes, and B. Hille. Light scattering and birefringence changes during nerve activity. Nature 218: 438–441, 1968.
 37. Cohen, L. B., R. D. Keynes, and D. Landowne. Changes in light scattering that accompany the action potential in squid giant axons: potential‐dependent components. J. Physiol. London 224: 701–725, 1972.
 38. Cohen, L. B., R. D. Keynes, and D. Landowne. Changes in axon light‐scattering that accompany the action potential: current dependent components. J. Physiol. London 224: 727–752, 1972.
 39. Cohen, L. B., B. M. Salzberg, H. V. Davila, W. N. Ross, D. Landowne, A. S. Waggoner, and C.‐H. Wang. Changes in axon fluorescence during activity: molecular probes of membrane potential. J. Membrane Biol. 19: 1–36, 1974.
 40. Colquhoun, D., R. Henderson, and J. M. Ritchie. The binding of labeled tetrodotoxin to non‐myelinated nerve fibres. J. Physiol. London 227: 95–126, 1972.
 41. Connelly, C. M. Recovery processes and metabolism of nerve. Rev. Mod. Physics 31: 475–484, 1959.
 42. Conti, F., and I. Tasaki. Changes in extrinsic fluorescence in squid axons during voltage‐clamp. Science 169: 1322–1324, 1970.
 43. Danforth, W. H., and D. Helmreich. Regulation of glycolysis in muscle. I. The conversion of phosphorylase b to phosphorylase a in frog sartorius muscle. J. Biol. Chem. 239: 3133–3138, 1964.
 44. Davila, H. V., L. B. Cohen, B. M. Salzberg, and B. B. Shrivastav. Changes in ANS and TNS fluorescence in giant axons from Loligo. J. Membrane Biol. 15: 29–46, 1974.
 45. Den Hertog, A., and J. M. Ritchie. A comparison of the effect of temperature, metabolic inhibitors and of ouabain on the electrogenic component of the sodium pump in mammalian non‐myelinated nerve fibres. J. Physiol. London 204: 523–538, 1969.
 46. De Weer, P. Aspects of the recovery processes in nerve. In: MTP International Review of Science. Physiology Series. Neurophysiology edited by C. C. Hunt. Baltimore: University Park Press, 1975, vol. 3, p. 231–278.
 47. De Weer, P., and D. Geduldig. Electrogenic sodium pump in squid giant axon. Science 179: 1326–1328, 1973.
 48. Doane, M. G. Fluorometric measurement of pyridine nucleotide reduction in the giant axon of the squid. J. Gen. Physiol. 50: 2603–2632, 1967.
 49. Dodge, F. A. A Study of Ionic Permeability Changes Underlying Excitation in Myelinated Nerve Fibers of the Frog (Ph.D. thesis). Ann Arbor: Rockefeller University, University Microfilms, Inc., No. 64–7333, 1963.
 50. Entine, G. Physical Probes of Nerve Membrane Structure (Ph.D. thesis). Berkeley: Univ. Calif., 1969.
 51. Fahn, S., S. J. Koval, and R. W. Albers. Sodium‐potassium‐activated adenosine triphosphatase of Electrophorus electric organ. I. An associated sodium‐activated transphosphorylation. J. Biol. Chem. 241: 1882–1889, 1966.
 52. Fenn, W. O. The oxygen consumption of frog nerve during stimulation. J. Gen. Physiol. 10: 767–779, 1927.
 53. Ferrendelli, J. A., and D. B. McDougal, Jr. The effect of audiogenic seizures on regional CNS energy reserves, glycolysis and citric acid cycle flux. J. Neurochem. 18: 1207–1220, 1971.
 54. Frank, G. M. Physical, chemical and structural processes during initiation and propagation of impulses through the nerve fiber. Izv. Akad. Nauk. SSSR Ser. Biol. 1: 26–38, 1958.
 55. Frankenhaeuser, B., and A. L. Hodgkin. The after‐effects of impulses in the giant nerve fibres of Loligo. J. Physiol. London 131: 341–376, 1956.
 56. Gage, P. W., and J. I. Hubbard. The origin of the posttetanic hyperpolarization of mammalian motor nerve terminals. J. Physiol. London 184: 335–352, 1966.
 57. Garrahan, P. J., and I. M. Glynn. The stoicheiometry of the sodium pump. J. Physiol. London 192: 217–235, 1967.
 58. Geren, B. B., and F. O. Schmitt. The structure of the Schwann cell and its relation to the axon in certain invertebrate nerve fibers. Proc. Natl. Acad. Sci. US 40: 863–870, 1954.
 59. Gilbert, D. L., and G. Ehrenstein. Use of a fixed charge model to determine the pK of the negative sites on the external membrane surface. J. Gen. Physiol. 55: 822–825, 1970.
 60. Gilter, C. Plasticity of biological membranes. Ann. Rev. Biophys. Bioengr. 1: 51–92, 1972.
 61. Girardier, L., J. P. Reuben, P. W. Brandt, and H. Grundfest. Evidence for anion‐permselective membrane in crayfish muscle fibers and its possible role in excitation‐contraction coupling. J. Gen. Physiol. 47: 189–214, 1963.
 62. Glassman, E. The biochemistry of learning: an evaluation of the role of RNA and protein. Ann. Rev. Biochem. 38: 605–646, 1969.
 63. Glynn, I. M. Activation of ATPase activity in a cell membrane by external K and internal sodium. J. Physiol. London 160: 18P, 1962.
 64. Glynn, I. M. Membrane adenosine triphosphatase and cation transport. Brit. Med. Bull. 24: 165–169, 1968.
 65. Godfraind‐De Becker, A. Heat production and fluorescence changes of toad sartorius muscle during aerobic recovery after a short tetanus. J. Physiol. London 223: 719–734, 1972.
 66. Goldring, J. M., and M. P. Blaustein. Synaptosome membrane potential changes monitored with a fluorescent probe (Abstract). San Diego, Calif.: Soc. Neurosci. 1973, p. 14–15.
 67. Golfand, K. A., Ja. Ju. Komissarchik, S. V. Levin, D. L. Rosenthal, and A. S. Troshin. The ultrastructure of the crab's axon and its permeability for vital dyes. Tsitolgiya 8: 585–597, 1966.
 68. Greengard, P., and R. W. Straub. Effect of frequency of electrical stimulation on the concentration of intermediary metabolites in mammalian nonmyelinated fibres. J. Physiol. London 148: 353–361, 1959.
 69. Härkönen, M. H. A., J. V. Passonneau, and O. H. Lowry. Relationships between energy reserves and function in rat superior cervical ganglia. J. Neurochem. 16: 1439–1450, 1969.
 70. Hill, A. V. The heat production of nerve. J. Pharmacol. Exptl. Therap. 29: 161–165, 1926.
 71. Hill, D. K. The effect of stimulation on the opacity of a crustacean nerve trunk and its relation to fibre diameter. J. Physiol. London 111: 283–303, 1950.
 72. Hill, D. K., and R. D. Keynes. Opacity changes in stimulated nerve. J. Physiol. London 108: 278–281, 1949.
 73. Hodgkin, A. L., and A. F. Huxley. Potassium leakage from an active nerve fibre. J. Physiol. London 106: 341–367, 1947.
 74. Hodgkin, A. L., and A. F. Huxley. Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo. J. Physiol. London 116: 449–472, 1952.
 75. Hodgkin, A. L., and A. F. Huxley. A quantitative description of membrane current and its application to conduction and excitation in nerve. J. Physiol. London 117: 500–544, 1952.
 76. Hodgkin, A. L., A. F. Huxley, and B. Katz. Measurement of current‐voltage relations in the membrane of the giant axon of Loligo. J. Physiol. London 116: 424–448, 1952.
 77. Hodgkin, A. L., and R. D. Keynes. Active transport of cations in giant axons from Sepia and Loligo. J. Physiol. London 128: 28–60, 1955.
 78. Hodgkin, A. L., and R. D. Keynes. Movements of labelled calcium in squid giant axons. J. Physiol. London 138: 253–281, 1957.
 79. Hoffman, J. F., and P. G. Laris. Determination of membrane potentials in human and amphiuma red blood cells using a fluorescent probe. J. Physiol. London. 239: 519–552, 1974.
 80. Howarth, J. V., R. D. Keynes, and J. M. Ritchie. The origin of the initial heat associated with a single impulse in mammalian non‐myelinated nerve fibres. J. Physiol. London 194: 745–793, 1968.
 81. Jansen, J. K. S., and J. G. Nicholls. Conductance changes, an electrogenic pump and the hyperpolarization of leech neurones following impulses. J. Physiol. London 229: 635–655, 1973.
 82. Jöbsis, F. J., and J. C. Duffield. Oxidative and glycolytic recovery metabolism in muscle. Fluorometric observations on their relative contributions. J. Gen. Physiol. 50: 1009–1047, 1967.
 83. Johnson, S. M., and A. D. Bangham. The action of anaesthetics on phospholipid membranes. Biochim. Biophys. Acta 193: 92–104, 1969.
 84. Karpatkin, S., E. Helmreich, and C. F. Cori. Regulation of glycolysis in muscle. II. Effect of stimulation and epinephrine in isolated frog sartorius muscle. J. Biol. Chem. 239: 3139–3145, 1964.
 85. Kay, H. F. Electrostriction and piezoelectricity. In: Encyclopaedic Dictionary of Physics, edited by J. Thewlis. New York: Pergamon, 1961, vol. 2, p. 835–840.
 86. Kemp, R. G. Rabbit liver phosphofructokinase. Comparison of some properties with those of muscle phosphofructokinase. J. Biol. Chem. 246: 245–252, 1971.
 87. Kerker, M. The Scattering of Light and Other Electromagnetic Radiation. New York: Academic, 1969.
 88. Keynes, R. D. The leakage of radioactive potassium from stimulated nerve. J. Physiol. London 113: 99–114, 1951.
 89. Keynes, R. D., and P. R. Lewis. The sodium and potassium content of cephalopod nerve fibres. J. Physiol. London 114: 151–182, 1951.
 90. Keynes, R. D., and J. M. Ritchie. The movements of labelled ions in mammalian non‐myelinated nerve fibres. J. Physiol. London 179: 333–367, 1965.
 91. King, L. J., O. H. Lowry, J. V. Passonneau, and V. Venson. Effects of convulsants on energy reserves in the cerebral cortex. J. Neurochem. 14: 599–611, 1967.
 92. Komissarchik, Ja. Ju., S. V. Levin, D. L. Rozenthal, and A. S. Troshin. On structural changes in membranes of nerve fibres. Ukr. Biokim. Zh. 43: 166–172, 1971.
 93. Kostyuk, P. G., O. A. Krishtal, and V. I. Pidoplichko. Potential dependent membrane current during the active transport of ions in snail neurones. J. Physiol. London 226: 373–392, 1972.
 94. Kregenow, F. M., and J. F. Hoffman. Some kinetic and metabolic characteristics of calcium‐induced potassium transport in human red cells. J. Gen. Physiol. 60: 406–429, 1972.
 95. Krnjević, K., and A. Lisiewicz. Injections of calcium ions into spinal motoneurones. J. Physiol. London 225: 363–390, 1972.
 96. Krzanowski, J., and F. M. Matchinsky. Regulation of phosphofructokinase by phosphocreatine and phosphorylated glycolytic intermediates. Biochem. Biophys. Res. Commun. 34: 816–823, 1969.
 97. Kuno, M., J. T. Miyahara, and J. N. Weakly. Post‐tetanic hyperpolarization produced by an electrogenic pump in dorsal spinocerebellar tract neurones of the cat. J. Physiol. London 210: 839–855, 1970.
 98. Landowne, D. Movement of sodium ions associated with the nerve impulse. Nature 242: 457–459, 1973.
 99. Landowne, D., and J. M. Ritchie. The binding of tritiated ouabain to mammalian non‐myelinated nerve fibres. J. Physiol. London 207: 529–537, 1970.
 100. Landowne, D., and J. M. Ritchie. Optical studies on the kinetics of the sodium pump in mammalian non‐myelinated nerve fibres. J. Physiol. London 212: 483–502, 1971.
 101. Landowne, D., and J. M. Ritchie. On the control of glycogenolysis in mammalian nervous tissue by calcium. J. Physiol. London 212: 503–517, 1971.
 102. Le Fèvre, C. G., and R. J. W. Le Fèvre. The Kerr effect. In: Physical Methods of Organic Chemistry, Part III, edited by A. Weissberger. New York: Interscience, 1960, p. 2459–2496.
 103. Lehninger, A. Mitochondria and calcium ion transport. Biochem. J. 119: 129–138, 1970.
 104. Levin, S. V., D. L. Rozenthal, K. A. Golfand, and Ja. Ju. Komissarchik. Changes in sorption of phthalocyanine dye (Heliogen blue SBL) by axon membranes of the crab during excitation. Tsitologiya 10: 312–321, 1968.
 105. Levin, S. V., D. L. Rozenthal, and Ja. Ju. Komissarchik. Structural changes in the axon membrane on excitation. Biofizika 13: 180–182, 1968.
 106. Lowry, O. H., and J. V. Passonneau. The relationship between substrates and enzymes of glycolysis in brain. J. Biol. Chem. 239: 31–42, 1964.
 107. Lowry, O. H., and J. V. Passonneau. Kinetic evidence for multiple binding sites on phosphofructokinase. J. Biol. Chem. 241: 2268–2279, 1966.
 108. Lowry, O. H., and J. V. Passonneau. A Flexible System of Enzymatic Analysis. New York: Academic, 1972.
 109. Lowry, O. H., J. V. Passonneau, F. X. Hasselberger, and D. W. Schulz. Effect of ischemia on known substrates and cofactors of the glycolytic pathway in brain. J. Biol. Chem. 239: 18–30, 1964.
 110. Ludkovskaya, R. G. Some structural and chemical phenomena in the stimulated neurone. Biofizika 2: 589–601, 1957.
 111. Masters, B. R., and D. M. Easton. Fluorescence changes of garfish olfactory nerve in relation to single electrical stimu lation. In: Abstracts of Contributed Papers. Fourth Internatinal Biophysics Congress, Moscow, 1972, vol. 3, p. 251.
 112. Meech, R. The sensitivity of Helix aspersa neurones to injected calcium ions. J. Physiol. London 237: 259–277, 1974.
 113. Meunier, J. M. Activation de la pompe à sodium dans les neurones géants d'aplysie. J. Physiol. Paris 63: 254A, 1971.
 114. Meves, H. Die Nachpotentiale isolierten markhaltigen Nervenfasern des Forsches bei tetanischer Reizung. Pfluegers Arch Ges. Physiol. 272: 336–359, 1961.
 115. Meyer, W. L., E. H. Fischer, and E. G. Krebs. Activation of skeletal muscle phosphorylase b kinase by Ca2+. Biochemistry 3: 1033–1039, 1964.
 116. Mitchison, J. M. A polarized light analysis of the human red cell ghost. J. Exptl. Biol. 30: 397–432, 1953.
 117. Montant, P., and M. Chmouliovsky. Energy‐rich metabolites in stimulated mammalian non‐myelinated nerve fibres. Experientia 24: 782–783, 1965.
 118. Moore, J. W., T. Narahashi, and T. I. Shaw. An upper limit to the number of sodium channels in nerve membrane. J. Physiol. London 188: 99–105, 1967.
 119. Mullins, L. J., and F. J. Brinley, Jr. Some factors influencing sodium extrusion by internally dialyzed squid axons. J. Gen. Physiol. 50: 2333–2355, 1967.
 120. Mullins, L. J., and F. J. Brinley, Jr. Substrate requirements for the operation of the Na pump. Abstr. Biophys. Soc. Meeting, Pittsburgh, Pa., 1968, p. 168a.
 121. Mullins, L. J., and F. J. Brinley, Jr. Potassium fluxes in dialyzed squid axons. J. Gen. Physiol. 53: 704–740, 1969.
 122. Nakajima, S., and K. Takahashi. Post‐tetanic hyperpolarization and electrogenic Na pump in stretch receptor neurone of crayfish. J. Physiol. London 187: 105–127, 1966.
 123. Nasonov, D. N. Local Reaction of Protoplasm and Propagation of Excitation. Moscow‐Leningrad: Acad. Sci. USSR, 1958. [Translated by Israel Program for Scientific Translations, Jerusalem, 1962.]
 124. Okada, Y., and D. B. McDougal, Jr. Physiological and biochemical changes in frog sciatic nerve during anoxia and recovery. J. Neurochem. 18: 2335–2353, 1971.
 125. Ørskov, S. L. Untersuchungen über den Einfluss von Kohlensäure und Blei auf die Permeabilität der Blutkörperchen für Kalium und Rubidium. Biochem. Z. 279: 250–261, 1935.
 126. Parker, C. A. Photoluminescence of Solutions. Amsterdam: Elsevier, 1968.
 127. Passonneau, J. V., and O. H. Lowry. Phosphofructokinase and the Pasteur effect. Biochem. Biophys. Res. Commun. 7: 10–15, 1962.
 128. Post, R. L., S. Kume, T. Tobin, B. Orcutt, and A. K. Sen. Flexibility of an active center in sodium‐plus‐potassium adenosine triphosphatase. J. Gen. Physiol. 54: 306S–326S, 1969.
 129. Radda, G. K. The design and use of fluorescent probes for membrane studies. Current Topics Bioenerg. 4: 81–126, 1971.
 130. Rang, H. P., and J. M. Ritchie. The dependence on external cations of the oxygen consumption of mammalian non‐myelinated fibres at rest and during activity. J. Physiol. London 196: 163–181, 1968.
 131. Rang, H. P., and J. M. Ritchie. On the electrogenic sodium pump in mammalian non‐myelinated nerve fibres and its activation by various external cations. J. Physiol. London 196: 183–221, 1968.
 132. Reuter, H. Divalent cations as charge carriers in excitable membranes. Prog. Biophys. Mol. Biol. 26: 1–43, 1973.
 133. Riesen, A. H. Sensory deprivation. Progr. Physiol. Psychol. 1: 117–147, 1966.
 134. Ritchie, J. M. The oxygen consumption of mammalian nonmyelinated nerve fibres at rest and during activity. J. Physiol. London 188: 309–329, 1967.
 135. Ritchie, J. M. Electrogenic ion pumping in nervous tissue. Current Topics Bioenerg. 4: 327–356, 1971.
 136. Ritchie, J. M. Energetic aspects of nerve conduction: the relationships between heat production, electrical activity and metabolism. Progr. Biophys. Mol. Biol. 26: 147–187, 1973.
 137. Rolleston, F. S., and E. A. Newsholme. Control of glycolysis in cerebral cortex slices. Biochem. J. 104: 524–533, 1967.
 138. Sacktor, B., and E. C. Hurlbut. Regulation of metabolism in working muscle in vivo. II. Concentrations of adenine nucleotides, organic phosphate, and inorganic phosphate in insect flight muscle during flight. J. Biol. Chem. 241: 632–634, 1966.
 139. Sacktor, B., and E. Wormser‐Shavit. Regulation of metabolism in working muscle in vivo. I. Concentrations of some glycolytic, tricarboxylic acid cycle, and amino acid intermediates in insect flight muscle during flight. J. Biol. Chem. 241: 624–631, 1966.
 140. Salzberg, B. M., H. V. Davila, and L. B. Cohen. Optical recordings of impulses in individual neurons of an invertebrate central nervous system. Nature 246: 508–509, 1973.
 141. Schmitt, F. O., and R. S. Bear. The optical properties of vertebrate axons as related to fiber size. J. Cell. Comp. Physiol. 9: 261–273, 1937.
 142. Sen, A. K., and R. L. Post. Stoichiometry and localization of adenosine triphosphate‐dependent sodium and potassium transport in the erythrocyte. J. Biol. Chem. 239: 345–352, 1964.
 143. Shanes, A. M. Effect of temperature on potassium liberation during nerve activity. Am. J. Physiol. 177: 377–382, 1954.
 144. Sims, P. J., A. S. Waggoner, C. H. Wang, and J. F. Hoffman. Studies on the mechanism by which cyanine dyes measure membrane potential in red blood cells and phosphatidylcholine vesicles. Biochemistry 13: 3315–3330, 1974.
 145. Skou, J. C. Local anaesthetics. VI. Relation between blocking potency and penetration of a monomolecular layer of lipids from nerves. Acta Pharmacol. Toxicol. 10: 325–337, 1954.
 146. Skou, J. C. The influence of some cations on an adenosine triphosphatase from peripheral nerves. Biochim. Biophys. Acta 23: 394–401, 1957.
 147. Skou, J. C. Relation between the ability of various compounds to block nervous conduction and their penetration into a monomolecular layer of nerve‐tissue lipoids. Biochim. Biophys. Acta 30: 625–629, 1958.
 148. Skou, J. C. Sequence of steps in the (Na + K)‐activated enzyme system in relation to sodium and potassium transport. Current Topics Bioenerg. 4: 357–398, 1971.
 149. Takenaka, T., R. Hirakow, and S. Yamagishi. Ultrastructural examination of the squid giant axons perfused intracellularly with protease. J. Ultrastruct. Res. 25: 408–416, 1968.
 150. Tanford, C. Physical Chemistry of Macromolecules. New York; Wiley, 1961, p. 278.
 151. Tasaki, I., E. Carbone, K. Sisco, and I. Singer. Spectral analyses of extrinsic fluorescence of the nerve membrane labeled with amino‐naphthalene derivatives. Biochim. Biophys. Acta 323: 220–233, 1973.
 152. Tasaki, I., L. Carnay, R. Sandlin, and A. Watanabe. Fluorescence changes during conduction in nerves stained with acridine orange. Science 163: 683–685, 1969.
 153. Tasaki, I., L. Carnay, and A. Watanabe. Transient changes in extrinsic fluorescence of nerve produced by electric stimulation. Proc. Natl. Acad. Sci. US 64: 1362–1368, 1969.
 154. Tasaki, I., M. Hallett, and E. Carbone. Further studies of nerve membranes labeled with fluorescent probes. J. Membrane Biol. 11: 353–376, 1973.
 155. Tasaki, I., A. Watanabe, and M. Hallett. Fluorescence of squid axon membrane labelled with hydrophobic probes. J. Membrane Biol. 8: 109–132, 1972.
 156. Tasaki, I., A. Watanabe, R. Sandlin, and L. Carnay. Changes in fluorescence, turbidity, and birefringence asso ciated with nerve excitation. Proc. Natl. Acad. Sci. US 61: 883–888, 1968.
 157. Thomas, R. C. Membrane current and intracellular sodium changes in a snail neurone during extrusion of injected sodium. J. Physiol. London 201: 495–514, 1969.
 158. Thomas, R. C. Electrogenic sodium pump in nerve and muscle cells. Physiol. Rev. 52: 563–594, 1972.
 159. Tobias, J. M., and P. G. Nelson. Structure and function in nerve. In: A Symposium on Molecular Biology, edited by R. E. Zirkle. Chicago: Univ. Chicago Press, 1959, p. 248–265.
 160. Villegas, G. M., and R. Villegas. Ultrastructural studies of squid nerve fibers. J. Gen. Physiol. 51: 44s–60s, 1968.
 161. Von Muralt, A. “Optical spike” during excitation in peripheral nerve. Abstr. Intern. Physiol. Congr. 25th, Munich, 1971, p. 638.
 162. Watanabe, A., S. Terakawa, and M. Nagano. Axoplasmic origin of the birefringence change associated with excitation of a crab nerve. Proc. Japan Acad. 49: 470–475, 1973.
 163. Williamson, J. R. Glycolytic control mechanisms. II. Kinetics of intermediate changes during the aerobic‐anoxic transition in perfused rat heart. J. Biol. Chem. 241: 5026–5036, 1966.
 164. Williamson, J. R., W. Y. Cheung, H. S. Coles, and B. E. Herczeg. Glycolytic control mechanisms. IV. Kinetics of glycolytic intermediate changes during electrical discharge and recovery in the main organ of Electrophorus electricus. J. Biol. Chem. 242: 5112–5118, 1967.
 165. Williamson, J. R., B. E. Herczeg, H. S. Coles, and W. Y. Cheung. Glycolytic control mechanisms. V. Kinetics of high energy phosphate intermediate changes during electrical discharge and recovery in the main organ of Electrophorus electricus. J. Biol. Chem. 242: 5119–5124, 1967.

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L. B. Cohen, P. De Weer. Structural and Metabolic Processes Directly Related to Action Potential Propagation. Compr Physiol 2011, Supplement 1: Handbook of Physiology, The Nervous System, Cellular Biology of Neurons: 137-159. First published in print 1977. doi: 10.1002/cphy.cp010105