Abstract
γ-Aminobutyric acid (GABA)-mediated synaptic potentials in rat dorsal striatum in vitro were reduced in amplitude by the GABA B receptor agonists baclofen and 3-aminopropyl-(methyl)-phosphinic acid (SK&F 97541), without any detectable postsynaptic effect. Synaptic potentials in 40% of neurones were distinctly multiphasic, the components of which exhibited a differential sensitivity to GABA B agonists. One population of GABA-releasing neurones within the striatum had presynaptic GABA B autoreceptors, whereas others were not directly affected by GABA B agonists.
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