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 state-dependent potential appears to be generated, at least in part, by cholinergic pedunculopontine nucleus projections. The present studies used localized microinjections of neuroactive compounds into the region of the pedunculopontine nucleus in order to modulate the vertex-recorded P13 potential. Both the GABAergic agonist, muscimol, and the noradrenergic alpha(2) receptor agonist, clonidine, were found to reduce the amplitude of the P13 potential in a dose-dependent manner. The suppressive effect of clonidine on P13 potential amplitude was blocked by pretreatment with the noradrenergic at receptor antagonist, yohimbine. In addition, habituation of the P13 potential, measured using a paired stimulus paradigm, was increased by microinjection 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, microinjection of yohimbine decreased habituation of the P13 potential. These results show that the vertex-recorded P13 potential and its habituation can be modulated by activation of known inhibitory synapses, both GABAergic and noradrenergic, at the level of the pedunculopontine nucleus. This provides further evidence that the P13 potential is generated, at least in part, by pedunculopontine nucleus outputs. (C) 1999 IBRO. Published by Elsevier Science Ltd.