HETEROGENEITY IN USE-DEPENDENT DEPRESSION OF INHIBITORY POSTSYNAPTIC POTENTIALS IN THE RAT NEOSTRIATUM IN-VITRO

''Minimal stimulation'' was applied to evoke responses in an ''all-or- none'' fashion in presumed medium spiny neurons of rat neostriatal sli ces in the presence of antagonists for glutamatergic excitation. For c omparison, responses were evoked in the same cells by compound stimula tion. Bicuculline (30 mu M) blocked responses evoked by minimal stimul ation, indicating that they were gamma-aminobutyric acid-A (GABA(A))-r eceptor-mediated inhibitory postsynaptic potentials (IPSPs), whereas r esponses evoked by compound stimulation were only reduced in amplitude . Likewise, R(-)baclofen (1-20 mu M) blocked IPSPs evoked by minimal s timulation in all but one cell. On the contrary, responses evoked by c ompound stimulation were always reduced in amplitude but never blocked . Paired-pulse depression (PPD) of averaged responses to minimal and c ompound stimulation was observed at a stimulus interval of 300 ms. The GABA(B) receptor antagonist CGP55845A (0.5 mu M) had no effect on PPD evoked by compound stimulation but abolished PPD evoked by minimal st imulation. In a second set of experiments, the two stimulation paradig ms were used to evoke responses in neostriatal slices continuously bat hed in R(-)baclofen (10-20 mu M). In R(-)baclofen a strong PPD was evo ked by minimal and by compound stimulation. The amplitude of the respo nse to compound stimulation increased on application of CGP55845A (0.5 mu M). At the same time, PPD evoked by compound stimulation decreased . On the contrary, IPSP amplitude and PPD evoked by minimal stimulatio n remained unchanged. We conclude that two types of GABAergic terminal s exist in the rat neostriatum, only one of which is regulated by GABA (B) receptors. However, the other class of terminals, not regulated by GABA(B) receptors, displays a much more pronounced PPD.