Premium
Stimulus‐secretion coupling in porcine adrenal chromaffin cells: Effect of dexamethasone
Author(s) -
Fuller Lynn Z.,
Lu Chengbiao,
McMahon Douglas G.,
Lindemann Merlin D.,
Jorgensen Mark S.,
Rau Shane W.,
Sisken Jesse E.,
Jackson Brian A.
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19970815)49:4<416::aid-jnr3>3.0.co;2-b
Subject(s) - endocrinology , medicine , depolarization , chromaffin cell , catecholamine , intracellular , adrenal medulla , long term potentiation , agonist , secretion , chemistry , acetylcholine , cytosol , biology , receptor , biochemistry , enzyme
Recent studies from this laboratory established that dexamethasone (DEX) potentiates Ca 2+ current via voltage‐gated Ca 2+ channels (VGCC), and as a consequence potentiates agonist‐induced cytosolic Ca 2+ transients in rat adrenal chromaffin cells. The present study examined whether DEX can also modulate VGCC activity and agonist‐induced cytosolic Ca 2+ transients in porcine adrenal medullary chromaffin (PAMC) cells, and if so whether this results in alterations in catecholamine secretion. Forty‐eight‐hr exposure to 1 μM DEX significantly increased peak Ca 2+ current (Δ + 138%; n = 6; P < 0.05) in PAMC cells. DEX treatment also significantly potentiated the increase in cytosolic Ca 2+ in response to membrane depolarization with KCl (Δ + 20%; n = 29; P < 0.05), but did not affect the amplitude of Ca 2+ transients elicited by nicotine or acetylcholine. Despite the potentiation of intracellular Ca 2+ , DEX treatment had no effect on KCl‐induced secretion of either norepinephrine or epinephrine. These data demonstrate that as in the rat chromaffin cell, DEX can also increase VGCC activity in PAMC cells. However, the subsequent potentiation of selected agonist‐induced increases in intracellular Ca 2+ does not appear to be sufficient to alter catecholamine secretion. J. Neurosci. Res. 49:416–424, 1997. © 1997 Wiley‐Liss, Inc.