Effect of alpha2 antagonists and an agonist on EEG slowing induced by scopolamine and lesion of the nucleus basalis.

In the present study, the effects of an alpha 2 agonist (clonidine, 1.0 mg/kg i.p.) and two antagonists (atipamezole, 1 and 10 mg/kg s.c. and yohimbine, 3.0 mg/kg i.p.) were studied on the EEG activity of naive rats, pretreated with either saline or scopolamine (0.8 mg/kg), or rats receiving lesioning of the nucleus basalis. The alpha 2 antagonists increased fast activity (alpha and beta). Clonidine increased slow wave activity (increased in spectral amplitudes) during periods of immobility and mobility. The EEG slowing, induced by scopolamine, was not alleviated by antipamezole or yohimbine, but in immobile rats, an increase in the delta and theta amplitudes was augmented by clonidine. In nucleus basalis-lesioned rats, the increase in delta activity was partially normalised by the alpha 2 antagonists. The decrease in the beta amplitude, induced by lesioning of the nucleus basalis, was not alleviated with either atipamezole or yohimbine. Clonidine increased the slow wave activity in nucleus basalis-lesioned rats and induced an increase in delta and theta bands during immobility. No changes were induced by clonidine in the EEG recorded from rats with lesions of the nucleus basalis.