Neurochemical modulation of the P13 midlatency auditory evoked potential in the rat

be the rodent equivalent of the human P1 (or P50) potential. This sleep sta te-dependent potential appears to be generated, at least in part, by cholin ergic pedunculopontine nucleus projections. The present studies used locali zed microinjections of neuroactive compounds into the region of the peduncu lopontine nucleus in order to modulate the vertex-recorded P13 potential. B oth the GABAergic agonist, muscimol, and the noradrenergic alpha(2) recepto r agonist, clonidine, were found to reduce the amplitude of the P13 potenti al in a dose-dependent manner. The suppressive effect of clonidine on P13 p otential amplitude was blocked by pretreatment with the noradrenergic at re ceptor antagonist, yohimbine. In addition, habituation of the P13 potential , measured using a paired stimulus paradigm, was increased by microinjectio n of a dose of muscimol or clonidine which did not change the amplitude of the P13 potential induced by the first stimulus of a pair. In contrast, mic roinjection of yohimbine decreased habituation of the P13 potential. These results show that the vertex-recorded P13 potential and its habituati on can be modulated by activation of known inhibitory synapses, both GABAer gic and noradrenergic, at the level of the pedunculopontine nucleus. This p rovides further evidence that the P13 potential is generated, at least in p art, by pedunculopontine nucleus outputs. (C) 1999 IBRO. Published by Elsev ier Science Ltd.