INHIBITION BY APOMORPHINE OF THE POTASSIUM‐EVOKED RELEASE OF [3H]‐γ‐AMINOBUTYRIC ACID FROM THE RAT SUBSTANTIA NIGRA in vitro

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Abstract
1 The spontaneous and potassium-evoked release of tritium from the rat substantia nigra prelabelled with [3H]-γ-aminobutyric acid [3H]-GABA were assessed in vitro under conditions of supervision 2 Kainic acid lesions performed in the right caudate nucleus resulted in a 70% reduction in the ability of the homolateral nigral cells to take up and retain [3H]-GABA when compared with the unlesioned side. The potassium-evoked release of [3H]-GABA remained proportional to the radioactivity retained in the tissue suggesting that the nigral GABA neurones that survived kainic acid treatment were still functional 3 The spontaneous outflow of [3H]-GABA was significantly increased by exposure to different concentrations of exogenous GABA (10 to 1000 μM) when amino-oxyacetic acid was present in the incubation medium 4 Apomorphine in concentrations ranging from 1 to 30 μM inhibited the calcium-dependent release of [3H]-GABA induced by 1 min exposure to 30 mM K+. These concentrations of apomorphine did not affect the spontaneous outflow of radioactivity. In vivo administration of haloperidol 0.2 mg/kg antagonized the in vitro inhibition by apomorphine of the K+-evoked release of [3H]-GABA 5 The results obtained with apomorphine and haloperidol suggest the presence of presynaptic dopamine-like inhibitory receptors in gabaergic nerve terminals 6 Dopamine in concentrations ranging up to 300 μM did not modify either the spontaneous or the K+-evoked release of [3H]-GABA from the substantia nigra. These concentrations of dopamine effectively displaced [3H]-dopamine recently taken up into the substantia nigra 7 Our results do not support the view that dendritic release of dopamine from the substantia nigra might be involved in the physiological modulation of the spontaneous or the stimulation-evoked release of GABA.