PHARMACOLOGICAL CHARACTERIZATION OF PRE-AND POSTSYNAPTIC GABA(B) RECEPTORS IN THE DEEP NUCLEI OF RAT CEREBELLAR SLICES

Whole-cell current- and voltage-clamp recordings were made from deep n uclear neurons in cerebellar slices from seven- to nine-day-old rats. Baclofen, a GABA(B) agonist, produced a slow postsynaptic hyperpolariz ation associated with a decrease in input resistance. The hyperpolariz ation was G-protein-dependent, blocked by intracellular Cs+ and antago nized by CGP 35348, a GABA(B) antagonist. In dialysed neurons recorded with Cs+-containing pipettes, baclofen suppressed deep nuclear neuron al inhibitory postsynaptic potentials and inhibitory postsynaptic curr ents evoked by electrical stimulations of the Purkinje cell axons. Thi s effect was blocked by CGP 35348, indicating that the suppressions we re mediated by presynaptic GABA(B) receptors. The inability of CGP 353 48 or uptake inhibitors (nipecotic acid and NO-711) to alter the decay of inhibitory postsynaptic currents evoked by maximal stimulation sug gested that GABA(B) receptors are not activated by the stimulation of the GABAergic input. Paired-pulse depression of inhibitory postsynapti c currents was not blocked by CGP 35348. Moreover, neither uptake inhi bitors nor CGP 35348 produced any significant changes to the whole-cel l current produced by a tetanic stimulation of Purkinje cell axons, su ggesting that GABA(B) autoreceptors were also not activated by endogen ous GABA release. Our findings indicate that while pre- and postsynapt ic GABA(B) receptors are present in the deep nuclei of the rat cerebel lum, they are not activated by electrical stimulation of the Purkinje cell axons.