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Abstract
Whole-cell current-and voltage-clamp recordings were made from deep nuclear neurons
in cerebellar slices from seven- to nine-day-old rats. Baclofen, a GABAB agonist,
produced a slow postsynaptic hyperpolarization associated with a decrease in input
resistance. The hyperpolarization was G-protein-dependent, blocked by intracellular
Cs+ and antagonized by CGP 35348, a GABAB antagonist. In dialysed neurons recorded
with Cs+ -containing pipettes, baclofen suppressed deep nuclear neuronal inhibitory
postsynaptic potentials and inhibitory postsynaptic currents evoked by electrical
stimulations of the Purkinje cell axons. This effect was blocked by CGP 35348, indicating
that the suppressions were mediated by presynaptic GABAB receptors. The inability
of CGP 35348 or uptake inhibitors (nipecotic acid and NO-711) to alter the decay of
inhibitory postsynaptic currents evoked by maximal stimulation suggested that GABAB
receptors are not activated by the stimulation of the GABAergic input. Paired-pulse
depression of inhibitory postsynaptic currents was not blocked by CGP 35348. Moreover,
neither uptake inhibitors nor CGP 35348 produced any significant changes to the whole-cell
current produced by a tetanic stimulation of Purkinje cell axons, suggesting that
GABAB autoreceptors were also not activated by endogenous GABA release. Our findings
indicate that while pre- and postsynaptic GABAB receptors are present in the deep
nuclei of the rat cerebellum, they are not activated by electrical stimulation of
the Purkinje cell axons.