GABAERGIC INPUT TO CHOLINERGIC NUCLEUS BASALIS NEURONS

The potential influence of GABAergic input to cholinergic basalis neur ons was studied in guinea-pig basal forebrain slices. GABA and its ago nists were applied to electrophysiologically-identified cholinergic ne urons, of which some were labelled with biocytin and confirmed to be c holine acetyltransferase-immunoreactive. Immunohistochemistry for glut amate decarboxylase was also performed in some slices and revealed GAB Aergic varicosities in the vicinity of the biocytin-filled soma and de ndrites of electophysiologically-identified cholinergic cells. From re st (average - 63 mV), the cholinergic cells were depolarized by GABA. The depolarization was associated with a decrease in membrane resistan ce and diminution in firing. The effect was mimicked by muscimol, the specific agonist for GABA(A) receptors, and not by baclofen; the speci fic agonist For GABA(B) receptors, which had no discernible effect. Th e GABA- and muscimol-evoked depolarization and decrease in resistance were found to be postsynaptic since they persisted in the presence of solutions containing either high Mg2+/low Ca2+ or tetrodotoxin. They w ere confirmed as being mediated by a GABA(A) receptor, since they were antagonized by bicuculline. The reversal potential for the muscimol e ffect was estimated to be similar to - 45 mV, which was -15 mV above t he resting membrane potential. Finally, in some cholinergic cells, spo ntaneous subthreshold depolarizing synaptic potentials (average 5 mV i n amplitude), which were rarely associated with action potentials, wer e recorded and found to persist in the presence of glutamate receptor antagonists but to be eliminated by bicuculline. These results suggest that GABAergic input map be depolarizing, yet predominantly inhibitor y to cholinergic basalis neurons. (C) 1998 IBRO. Published by Elsevier Science Ltd.