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NMDA and Non‐NMDA Receptor‐Mediated Release of [ 3 H]GABA from Granule Cell Dendrites of Rat Olfactory Bulb
Author(s) -
García Y.,
Ibarra C.,
Jaffé E. H.
Publication year - 1995
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.1471-4159.1995.64020662.x
Subject(s) - kainate receptor , cnqx , nmda receptor , ampa receptor , glutamate receptor , chemistry , nipecotic acid , biology , pharmacology , biochemistry , biophysics , neurotransmitter , receptor
Abstract: We have studied the effect of glutamate and the glutamatergic agonists N ‐methyl‐ d ‐aspartate (NMDA), kainate, and α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) on [ 3 H]GABA release from the external plexiform layer of the olfactory bulb. The GABA uptake blocker nipecotic acid significantly increased the basal [ 3 H]GABA release and the release evoked by a high K + concentration, glutamate, and kainate. The glutamate uptake blocker pyrrolidine‐2,4‐dicarboxylate (2,4‐PDC) inhibited by 50% the glutamate‐induced [ 3 H]GABA release with no change in the basal GABA release. The glutamatergic agonists NMDA, kainate, and AMPA also induced a significant [ 3 H]GABA release. The presence of glycine and the absence of Mg 2+ have no potentiating effect on NMDA‐stimulated release; however, when the tissue was previously depolarized with a high K + concentration, a significant increase in the NMDA response was observed that was potentiated by glycine and inhibited by the NMDA receptor antagonist 2‐amino‐5‐phosphonoheptanoic acid (AP‐7). The kainate and AMPA effects were antagonized by the non‐NMDA receptor antagonist 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) but not by AP‐7. The glutamate effect was also inhibited by CNQX but not by the NMDA antagonist 2‐amino‐5‐phosphonopentanoic acid (AP‐5); nevertheless, in the presence of glycine, [ 3 H]GABA release evoked by glutamate was potentiated, and this response was significantly antagonized by AP‐5. Tetrodotoxin inhibited glutamate‐ and kainate‐stimulated [ 3 H]GABA release but not the NMDA‐stimulated release. The present results show that in the external plexiform layer of the olfactory bulb, glutamate is stimulating GABA release through a presynaptic, receptor‐mediated mechanism as a mixed agonist on NMDA and non‐NMDA receptors; glutamate is apparently also able to induce GABA release through heteroexchange.