Activation of nigral dopamine neurons by the selective GABA B -receptor antagonist SCH 50911

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Abstract
Previous studies have shown that systemic as well as local administration of the GABAB-receptor agonist baclofen is associated with a decrease in firing rate, a regularisation of firing rhythm and a decrease in burst firing activity of dopamine (DA) containing midbrain neurons. In the present electrophysiological study we have utilised the novel, selective and potent GABAB-receptor antagonist SCH 50911 in order to further analyse the importance of GABAB-receptors for the overall activity of rat nigral DA neurons. SCH 50911 given intravenously (1–64 mg/kg) or locally, by microiontophoretic techniques, was found to increase firing rate and to increase the burst firing activity of DA neurons. The present data suggest that the GABAB-receptor antagonist blocks somatodendritic receptors on nigral DA neurons. This GABA-receptor input appears to be of a tonic nature. It is proposed that the activation of nigral DA neurons may underlie the beneficial effects of GABAB-receptor antagonists in the modulation of cognition and that GABAB-receptor antagonists may be of therapeutic value in the treatment of Parkinson's disease.

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