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Calcium Signaling System in Salivary Glands

James W. Jr. Putney

10.1002/cphy.cp060303

Source: Supplement 18: Handbook of Physiology, The Gastrointestinal System, Salivary, Gastric, Pancreatic, and Hepatobiliary Secretion

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Stimulus‐Permeability Coupling in Salivary Glands
2 Phosphoinositides and Salivary Receptor Mechanisms
2.1 Phosphoinositide Turnover in Salivary Glands
2.2 Pathways of Phosphoinositide Turnover in Salivary Glands
2.3 Phosphoinositides and Intracellular Calcium Release
2.4 Mechanism of Action of 1,4,5‐IP3
2.5 Calcium Entry
2.6 Capacitative Calcium Entry in Parotid Gland
3 Conclusions
Figure 1. Figure 1.

Efflux of 86Rb from salivary gland. Ordinate values represent apparent first‐order rate coefficients (X100%). Agonist (i.e., acetylcholine) is present from 20 to 40 min. Solid line, Ca2+ present throughout. Dotted line, Ca2+ absent but restored from 30 to 40 min.

From Putney 65
Figure 2. Figure 2.

Structures of phosphatidylinositol (PI), phosphatidylinositol‐4‐phosphate (PIP), and phosphatidylinositol‐4,5‐bisphosphate (PIP2).
Figure 3. Figure 3.

Formation of [3H]inositol phosphates in parotid acinar cells during initial 60 s after addition of 10‐4 M methacholine. Closed circles, inositol monophosphate; open circles, inositol bisphosphate; open triangles, inositol trisphosphate. Values are means ± SE of 4 experiments. Control values did not change appreciably over 60‐s period.

From Aub and Putney 3
Figure 4. Figure 4.

Time course of inositol trisphosphate (IP3)‐stimulated Ca2+ mobilization. Isolated parotid acinar cells were permeabilized with saponin. CaCl2 was added and cells were allowed to reequilibrate, after which inositol‐1,4,5‐trisphosphate 1,4,5‐IP3) was added (t = 1 min). Change in quin 2 fluorescence was monitored as an indicator of changing free [Ca2+]. Excess Ca2+ was added after response was completed, followed by alkaline ethylene glycol‐bis(β‐aminoethylether)‐N,N'‐tetraacetic acid (EGTA) for calibration purposes. Representative traces for 3 concentrations of IP3 are superimposed; 0.3 μM, 1 μM, and 3 μM IP3 produced similarly graded increases in fluorescence.

From Aub 2
Figure 5. Figure 5.

Capacitative model for receptor regulation of Ca2+ release and entry. Agonist (Ag) binding to its receptor (RA) leads to breakdown of phosphatidylinositol‐4,5‐bisphosphate (PIP2) into diglyceride (DG) and inositol‐1,4,5‐trisphosphate 1,4,5‐IP3). 1,4,5‐IP3 binds to a receptor (R1) on the receptor‐regulated pool, presumably an endoplasmic reticulum component, which activates Ca2+ discharge to the cytosol and the Ca2+‐release phase of the response. Decrease in Ca2+ content of the pool relieves an inhibitory constraint on a direct pathway for Ca2+ to enter the pool from the extracellular space. With continued presence of 1,4,5‐IP3, Ca2+ continues down its concentration gradient to cytosol, resulting in a sustained Ca2+‐entry phase of the response.

From Putney 67


Figure 1.

Efflux of 86Rb from salivary gland. Ordinate values represent apparent first‐order rate coefficients (X100%). Agonist (i.e., acetylcholine) is present from 20 to 40 min. Solid line, Ca2+ present throughout. Dotted line, Ca2+ absent but restored from 30 to 40 min.

From Putney 65


Figure 2.

Structures of phosphatidylinositol (PI), phosphatidylinositol‐4‐phosphate (PIP), and phosphatidylinositol‐4,5‐bisphosphate (PIP2).



Figure 3.

Formation of [3H]inositol phosphates in parotid acinar cells during initial 60 s after addition of 10‐4 M methacholine. Closed circles, inositol monophosphate; open circles, inositol bisphosphate; open triangles, inositol trisphosphate. Values are means ± SE of 4 experiments. Control values did not change appreciably over 60‐s period.

From Aub and Putney 3


Figure 4.

Time course of inositol trisphosphate (IP3)‐stimulated Ca2+ mobilization. Isolated parotid acinar cells were permeabilized with saponin. CaCl2 was added and cells were allowed to reequilibrate, after which inositol‐1,4,5‐trisphosphate 1,4,5‐IP3) was added (t = 1 min). Change in quin 2 fluorescence was monitored as an indicator of changing free [Ca2+]. Excess Ca2+ was added after response was completed, followed by alkaline ethylene glycol‐bis(β‐aminoethylether)‐N,N'‐tetraacetic acid (EGTA) for calibration purposes. Representative traces for 3 concentrations of IP3 are superimposed; 0.3 μM, 1 μM, and 3 μM IP3 produced similarly graded increases in fluorescence.

From Aub 2


Figure 5.

Capacitative model for receptor regulation of Ca2+ release and entry. Agonist (Ag) binding to its receptor (RA) leads to breakdown of phosphatidylinositol‐4,5‐bisphosphate (PIP2) into diglyceride (DG) and inositol‐1,4,5‐trisphosphate 1,4,5‐IP3). 1,4,5‐IP3 binds to a receptor (R1) on the receptor‐regulated pool, presumably an endoplasmic reticulum component, which activates Ca2+ discharge to the cytosol and the Ca2+‐release phase of the response. Decrease in Ca2+ content of the pool relieves an inhibitory constraint on a direct pathway for Ca2+ to enter the pool from the extracellular space. With continued presence of 1,4,5‐IP3, Ca2+ continues down its concentration gradient to cytosol, resulting in a sustained Ca2+‐entry phase of the response.

From Putney 67
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Article Title: Calcium Signaling System in Salivary Glands
 

How to Cite

James W. Jr. Putney. Calcium Signaling System in Salivary Glands. Compr Physiol 2011, Supplement 18: Handbook of Physiology, The Gastrointestinal System, Salivary, Gastric, Pancreatic, and Hepatobiliary Secretion: 51-61. First published in print 1989. doi: 10.1002/cphy.cp060303