Premium
Specificity of the effects of neuroleptics on the release of glutamate from the rat amygdala
Author(s) -
Mott J.,
Sherman A. D.
Publication year - 1987
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430110310
Subject(s) - glutamate receptor , butyrophenone , chemistry , reserpine , haloperidol , chlorpromazine , liberation , pharmacology , calcium , medicine , endocrinology , dopamine , biochemistry , receptor , in vitro , organic chemistry
The purpose of this study was to determine if the depression of calcium‐dependent glutamate release from synaptosomes derived from the rat amygdala is specific to neuroleptics. To this end the effects of nine nonneuroleptic agents and nine previously untested neuroleptic agents (or isomers) on nondependent and calcium‐dependent glutamate release were determined by gas‐chromatographic and radioisotopic methods. All of the neuroleptics except reserpine depressed calcium‐dependent release at 10 −7 M with only a weak, inconsistent reduction of nonspecific release. None of the nonneuroleptic agents at concentrations of 10 −6 M 10 −5 M produced depression of calcium‐dependent release without also strongly depressing nonspecific release. Reserpine was without effect on release at concentrations as high as 10 −7 M. Also shown was that the representive neuroleptics Haloperidol, chlorpromazine, and clozapine depressed the calcium‐dependent release of glutamine‐derived glutamate to a greater extent over glucose derived glutamate. These data suggest that the specific depression of stimulus ‐ coupled glutamate release is not a characteristic of noneuroleptic compounds, but is highly associated with neuroleptics of the phenothiazine or butyrophenone classes.