Abstract
The onset of slow wave sleep may require an inhibition of histaminergic neurons by GABAergic afferents from the ventrolateral preoptic area. We have utilized electrophysiological methods in an in vitro brain slice preparation to examine the role of GABAB receptor activation in GABAergic synaptic inhibition in histaminergic neurons of the tuberomammillary nucleus. Tetrodotoxin blocked evoked GABAergic IPSPs but not miniature IPSPs or IPSCs. Evoked IPSPs varied in amplitude and exhibited failures of transmission. Baclofen reduced the amplitude of evoked IPSPs in all experiments and often caused an increase in failures of transmission. Responses elicited by application of exogenous GABA were insensitive to baclofen treatment. The action of baclofen was blocked by CGP-35348 (100 microm), a GABAB receptor antagonist, which also enhanced the amplitude of evoked IPSPs. The frequency of spontaneous and miniature IPSPs and IPSCs was reduced by baclofen. However, the amplitude distribution of mIPSCs was not altered. We conclude that GABA release onto TM neurons is under presynaptic control via GABAB receptors. This presynaptic control of transmission to tuberomammillary neurons may reduce inhibition, increasing histamine release and enhancing wakefulness.
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