Baclofen attenuates hyperpolarizing not depolarizing responses of caudate neurons in cat.

The effects of baclofen, a gamma-aminobutyric acid (GABA) analogue, were studied on the intracellular responses of caudate neurons to cortical and thalamic stimulation. Systemic or intracaudate injections of baclofen did not reduce the initial excitatory postsynaptic potential (EPSP) to these stimuli; however, it did completely block evoked hyperpolarizations. These results suggest that the GABA-b receptor (one possible site of baclofen action) is not found on the corticostriate synaptic terminals. Furthermore, our results clearly indicate that evoked hyperpolarizations recorded in caudate neurons are not the result of cortical disfacilitation.