Heterogeneity in use-dependent depression of inhibitory postsynaptic potentials in the rat neostriatum 'in-vitro'. Radnikow, Gabriele, Jutta Rohrbacher, Ulrich Misgeld. Physiologisches Institut der Universit[umlaut]at Heidelberg, Im Neuenheimer Feld 326, D-69120 Heidelberg, Germany.
APStracts 3:0221N, 1996.
`Minimal stimulation' was applied to evoke responses in an 'all-or-none' fashion in presumed medium spiny neurons of rat neostriatal slices in the presence of antagonists for glutamatergic excitation. For comparison, responses were evoked in the same cells by compound stimulation. Bicuculline (30 [mu]M) blocked responses evoked by minimal stimulation indicating that they were GABA A receptor mediated inhibitory postsynaptic potentials (IPSPs), while responses evoked by compound stimulation were only reduced in amplitude. Likewise, R(-)baclofen (1-20 [mu]M) blocked IPSPs evoked by minimal stimulation in all but one cell. On the contrary, responses evoked by compound stimulation were always reduced in amplitude but never blocked. Paired pulse depression (PPD) of averaged responses to minimal and compound 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 stimulation. In a second set of experiments, the two stimulation paradigms were used to evoke responses in neostriatal slices continuously bathed in R(-)baclofen (10-20 [mu]M). In R(-)baclofen a strong PPD was evoked by minimal and by compound stimulation. The amplitude of the response to compound stimulation increased upon 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 stimulation remained unchanged. We conclude that two types of GABAergic terminals 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.

Received 10 June 1996; accepted in final form 18 September 1996.
APS Manuscript Number J461-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996