Premium
Calcium Modulation of Activation and Desensitization of Nicotinic Receptors from Mouse Brain
Author(s) -
Booker T. K.,
Smith K. W.,
Dodrill C.,
Collins A. C.
Publication year - 1998
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 - 10.1046/j.1471-4159.1998.71041490.x
Subject(s) - receptor , calcium , chemistry , nicotinic agonist , desensitization (medicine) , endocrinology , alpha 4 beta 2 nicotinic receptor , medicine , agonist , acetylcholine receptor , biophysics , nicotinic acetylcholine receptor , biology , biochemistry , organic chemistry
The effects of extracellular calcium on functional properties of nicotinic receptors from mouse thalamus were investigated. Previous studies have reported that calcium modulates the function of several neuronal nicotinic receptors. A 86 Rb + ion efflux assay was developed to measure nicotinic receptor function from brain tissue, and data indicate that α 4 β 2 receptors may mediate this response. Using the 86 Rb + efflux assay, calcium effects on receptor activation, desensitization induced by high, activating and low, subactivating concentrations of agonist, and recovery from desensitization were examined. Effects of calcium on the kinetics of ligand binding were also investigated. Calcium modulated receptor activation by increasing the maximal response to nicotine in a concentration‐dependent manner, without affecting the EC 50 of nicotine. Barium, but not magnesium, mimicked the effects of calcium on receptor activation. The increase in receptor activation could not be explained by changes in the ratio of activatable to desensitized receptors as assessed by the kinetics of ligand binding. Desensitization following activation was unaffected by calcium. Calcium, barium, and magnesium, however, increased the potency of nicotine for desensitization induced by exposure to low, subactivating concentrations of nicotine. Recovery from desensitization was not modulated by calcium. These data suggest that calcium modulates various functional aspects of nicotinic receptors from mouse brain and may do so via different mechanisms.