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Desensitization to Nicotinic Cholinergic Agonists and K + , Agents That Stimulate Catecholamine Secretion, in Isolated Adrenal Chromaffin Cells
Author(s) -
Boksa P.,
Livett B. G.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb02726.x
Subject(s) - desensitization (medicine) , chromaffin cell , endocrinology , cholinergic , catecholamine , nicotinic agonist , nicotine , medicine , acetylcholine , chemistry , homologous desensitization , intracellular , adrenal medulla , biology , receptor , biochemistry
Desensitization of catecholamine (CA) release from cultured bovine adrenal chromaffin cells was studied to characterize the phenomenon of desensitization and to attempt an elucidation of the mechanism(s) involved in this phenomenon at the level of the isolated chromaffin cell. Prior exposure of chromaffin cells to nicotinic cholinergic agonists [acetylcholine (ACh) or nicotine] caused a subsequent depression or desensitization of CA release during restimulation of the cells with the same agonists. Rates of development of and recovery from nicotinic desensitization were in the minute time range and the magnitude of nicotinic desensitization of CA release was greater at 37°C than at 23°C. ACh‐ (or nicotine)‐induced desensitization was shown to be the result of two processes: (1) a Ca 2+ ‐dependent component of desensitization, possibly due to a depletion of intracellular CA stores and (2) a Ca 2+ ‐independent, depletion‐independent component of desensitization. Prior exposure of cultured chromaffin cells to an elevated concentration of K + also resulted in desensitization of K + ‐induced CA release in these cells. K + ‐induced desensitization was completely Ca 2+ ‐dependent and was shown to be the result, at least in part, of a mechanism that is independent of depletion of CA stores.