W. Morishita et Br. Sastry, PHARMACOLOGICAL CHARACTERIZATION OF PRE-AND POSTSYNAPTIC GABA(B) RECEPTORS IN THE DEEP NUCLEI OF RAT CEREBELLAR SLICES, Neuroscience, 68(4), 1995, pp. 1127-1137
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.