Action of apomorphine, bromocriptine and lergotrile onγ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

Abstract

The effect of three dopamine agonists, apomorphine, bromocriptine and lergotrile, was tested on the release ofγ-aminobutyric acid, (GABA) and acetylcholine (ACh) from tissue slices of rat nucleus accumbens and striatum. All three agentsin vitro caused a dose dependent depression of the K⁺-evoked release of [¹⁴C]-GABA in corpus striatum. This effect was also obtained followingin vivo drug application and when endogenous GABA release was determined. A similar depression of GABA release was obtained in the nucleus accumbens. Both dopamine and dibutyryl adenosine-3′∶5′-cyclic monophosphoric acid inhibited the K⁺-evoked release of [¹⁴C]-GABA in corpus striatum. This inhibitory effect was not reversed by sulpiride. Bromocriptine and lergotrile also depressed the K⁺-evoked release of [³H]-acetylcholine from tissue slices of corpus striatum but not nucleus accumbens, as has previously been demonstrated for dopamine and apomorphine. In contrast, sulpiride enhanced the release of [³H]-acetylcholine and molindone reversed the apomorphine inhibition of [³H]-acetylcholine release. These results indicate that dopaminergic agents may influence the release of both GABA and ACh in the corpus striatum but only GABA in the nucleus accumbens.