Evoked release of endogenous amino acids from rat striatal slices and its modulation

Abstract

The release of endogenous γ-aminobutyric acid (GABA), glutamate and aspartate stimulated by high K + was studied by superfusing rat striatal slices. Stimulation with 5 min of 30 mM K + was applied twice (S 1 and S 2) at a 20 min interval. The maximum release of GABA following stimulation was 40 (at S 1) and 26 (at S 2) times greater than the basal release. S 1 and S 2 each produced a maximum release of almost same magnitude for both glutamate and aspartate (about 2.5 times basal release). The removal of Ca 2+ from the perfusion medium reduced the maximum release of these amino acids by more than 80% without affecting basal release significantly. Striatal slices were next stimulated in the same way after the addition of apomorphine or haloperidol to the perfusion medium. Apomorphine, 10 or 100 μM, reduced the K +-evoked release of GABA (by 24% at S 1 and 35% at S 2 with 10 μM; by 37% at S 1 and 47% at S 2 with 100 μM) but failed to affect the simultaneous release of glutamate and aspartate. Haloperidol (1 μM) reduced the S 1-induced release of GABA but had no significant effect on the subsequent S 2-induced release. The evoked release of aspartate or glutamate did not respond significantly to haloperidol, but there was a tendency to a decrease in aspartate release similar to the decrease seen for GABA release, particularly with S 1. Based on these results, we discuss the property of GABA, aspartate and glutamate as neurotransmitters and the possible dopaminergic regulation of the release of these amino acids.