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Inhibition by Diazepam and γ‐Aminobutyric Acid of Depolarization‐Induced Release of [ 14 C]Cysteine Sulfinate and [ 3 H]Glutamate in Rat Hippocampal Slices
Author(s) -
Baba Akemichi,
Okumura Shigetoshi,
Mizuo Hiroyuki,
Iwata Heitaroh
Publication year - 1983
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.1471-4159.1983.tb12683.x
Subject(s) - glutamate receptor , aminobutyric acid , chemistry , diazepam , veratridine , neurotransmitter , excitatory postsynaptic potential , glutamic acid , muscimol , inhibitory postsynaptic potential , biochemistry , gamma aminobutyric acid , bicuculline , biophysics , amino acid , pharmacology , endocrinology , biology , agonist , gabaa receptor , sodium channel , sodium , receptor , organic chemistry
Effects of diazepam and γ‐aminobutyric acid‐related compounds on the release of [ 14 C]cysteine sulfinate and [ 3 H]glutamate from preloaded hippocampal slices of rat brain were examined by a superfusion method. Diazepam markedly inhibited the release of cysteine sulfinate and glutamate evoked either by high K + or veratridine without affecting that of other neurotransmitter candidates, e.g., γ‐aminobutyric acid, acetylcholine, noradrenaline, and dopamine; IC 50 values for the release of cysteine sulfinate and glutamate were about 20 and 7 μ M , respectively. γ‐Aminobutyric acid (1 to 10 μ M ) and muscimol (100 μ M ) significantly reduced high K + ‐stimulated release of glutamate. Bicuculline, which had no effect on the release at a concentration of 50 μ M by itself, antagonized the inhibitory effects of diazepam and γ‐aminobutyric acid on glutamate release. Similar results were obtained with the release of cysteine sulfinate except that a high concentration (100 μ M ) of γ‐aminobutyric acid was required for the inhibition. These results indicate the modulation by γ‐aminobutyric acid innervation of the release of excitatory amino acids in rat hippocampal formation, and also suggest that some of the pharmacological effects of diazepam may be a consequence of inhibition of excitatory amino acid transmission.