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Release of γ‐[ 3 H]Aminobutyric Acid from Rat Olfactory Bulb and Substantia Nigra: Differential Modulation by Glutamic Acid
Author(s) -
Jaffe E. H.,
Vaello M. L.
Publication year - 1989
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.1471-4159.1989.tb07255.x
Subject(s) - nipecotic acid , glutamate receptor , kainic acid , substantia nigra , kainate receptor , gabaergic , glutamate decarboxylase , medicine , aminooxyacetic acid , biology , glutamic acid , olfactory bulb , chemistry , gamma aminobutyric acid , endocrinology , biophysics , biochemistry , ampa receptor , neurotransmitter , inhibitory postsynaptic potential , amino acid , receptor , dopaminergic , dopamine , central nervous system , enzyme
We have studied the glutamate modulation of γ‐[ 3 H]aminobutyric acid ([ 3 H]GABA) release from GABAergic dendrites of the external plexiform layer of the olfactory bulb and from GABAergic axons of the substantia nigra. In the olfactory bulb, [ 3 H]GABA release was induced by high K + and kainate, and not by aspartate and glutamate alone. However, when the tissue was conditioned by a previous K + depolarization, glutamate and aspartate caused [ 3 H]GABA release. The effect of glutamate was significantly enhanced when the GABA uptake mechanism was blocked by nipecotic acid. N ‐Methyl‐D‐aspartate and quisqualate did not cause [ 3 H]GABA release under the same conditions. The acidic amino acid receptor antagonist 2‐amino‐4‐phosphonobutyric acid and the N ‐methyl‐D‐aspartate receptor antagonist 2‐amino‐5‐phosphonovaleric acid significantly inhibited the K + ‐glutamate‐ and the kainate‐induced [ 3 H]GABA release. Mg 2+ (5 m M ), which blocks the N ‐methyl‐D‐aspartate receptors, significantly inhibited the K + ‐glutamate‐induced but not the kainic acid‐induced [ 3 H]GABA release. The K + ‐glutamate‐stimulated release, but not the K + ‐stimulated [ 3 H]GABA release, was strongly inhibited by Na + ‐free solutions or by 300 n M tetrodotoxin. Apparently the glutamateinduced release of [ 3 H]GABA occurs through an interneuron because it is dependent on the presence of nerve conduction. In the substantia nigra no [ 3 H]GABA release was elicited by any of the glutamate agonists tested. The present results clearly differentiate between the effects of glutamate on the release of [ 3 H]GABA from the substantia nigra and from the olfactory bulb. It is possible that in the external plexiform layer of the olfactory bulb there is a mixed population of voltage‐dependent excitatory amino acid receptors, capable of modulating GABA release through an interneuron. In the substantia nigra glutamate does not modulate GABA release.