Glutamate receptor activation induces carrier mediated release of endogenous GABA from rat striatal slices

J. Wang, G. Lonart, K. M. Johnson

Research output: Contribution to journalArticle

11 Scopus citations


The regulation of striatonigral and striatopallidal GABAergic neurons by glutamatergic afférents is thought to play a critical role in normal basal ganglia function. Here we report that in striatal slices about 17% of K+-induced endogenous GABA release was Ca2+-independent and this could be blocked by a GABA transport inhibitor. Activation of N-methyl-D-aspartate (NMDA)- and quisqualate-sensitive receptors induced endogenous GABA efflux only in the presence of a GABA transaminase inhibitor; this efflux was inhibited by 60-80% with a GABA transport inhibiter. NMDA-induced GABA release was blocked by phencyclidine, Mg2+ and COS 19755. Quisqualate-induced GABA release was blocked completely by a combination of the metabotropic antagonist, L-AP3 and CNQX, a non-NMDA receptor antagonist. These data indicate that excitatory amino acid agonistsinduced GABA release is distinct from that induced by high K+ depolarization.

Original languageEnglish (US)
Pages (from-to)31-43
Number of pages13
JournalJournal of Neural Transmission
Issue number1-2
StatePublished - Jan 1 1996



  • Ampa receptors
  • Gaba release
  • Metabotropic receptors
  • Nmda receptors
  • Phencyclidine
  • Reverse transport

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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