Enhancement by GABA of glutamate depolarization-induced release from cerebellar nerve endings.
Cerebellar synaptosomes were superfused in the presence of D-[3H]aspartate (to label the glutamate 'reuptake pool') and [14C]glutamine (to label the 'new synthesis pool'). The depolarization-induced release of D-[3H]aspartate and of newly synthesized [14C]glutamate were potentiated by low concentrations of GABA (2--20 microM) or muscimol. The effect was probably mediated by the interaction of GABA with presynaptic GABA receptors localized in 'glutamergic' nerve endings, since it was antagonized by the GABA antagonists picrotoxin and bicuculline.
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D002531:Cerebellum / Q000187:drug effects*; D005971:Glutamates / Q000378:metabolism*; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects; D011963:Receptors, GABA-A; D009435:Synaptic Transmission / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D005971:Glutamates; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D011188:Potassium