Stress‐Induced Enhancement of Suppression of [3H]GABA Release from Striatal Slices by Presynaptic Autoreceptor

Abstract

The effect of cold and immobilization stress on presynaptic GABAergic autoreceptors was examined using the release of [³H]GABA (γ-aminobutyric acid) from slices of rat striatum. It was found that in vitro addition of γ-aminolevulinic acid, as well as GABA agonists such as muscimol and imidazoleacetic acid, exhibited a significant suppression of the striatal release of [³H]GABA evoked by the addition of high potassium, whereas γ-aminovaleric acid had no significant effects on the evoked release. These suppressive actions were antagonized invariably by the GABA antagonists, bicucul-line and picrotoxin, but not by the glycine antagonist, strychnine. Cholinergic agonists, such as pilocarpine and tetramethylammonium, also attenuated significantly the evoked release of [³H]GABA from striatal slices, while none of its antagonists, including atropine, hexame-thonium and d-tubocurarine, affected the release. On the other hand, in vitro addition of dopamine receptor agents such as dopamine, apomorphine, and haloperidol, or the inhibitory amino acids, glycine, γ-alanine, and taurine failed to influence the evoked release of [³H]GABA from striatal slices. Application of a cold and immobilization stress for 3 h was found to induce a significant enhancement of the suppressive effects by muscimol and γ-aminolevulinic acid on the evoked release of [³H]GABA, without affecting that by pilocarpine and tetramethylammonium. These results suggest that the release of GABA from striatal GABA neurons may be regulated by presynaptic autoreceptors for this neuroactive amino acid, and may play a significant functional role in the exhibition of various symptoms induced by stress.