POWER SPECTRAL-ANALYSIS OF ELECTROENCEPHALOGRAPHIC DESYNCHRONIZATION INDUCED BY COCAINE IN RATS - CORRELATION WITH EVALUATION OF NORADRENERGIC NEUROTRANSMISSION AT THE MEDIAL PREFRONTAL CORTEX

We applied continuous, on-line and real-time spectral analysis of elec tro-encephalographic (EEG) signals and microdialysis to evaluate the p ossible participation of noradrenergic neurotransmission at the medial prefrontal cortex (mPFC) in EEG desynchronization induced by cocaine. Male Sprague-Dawley rats that were under chloral hydrate anesthesia w ere used. Intravenous administration of cocaine (1.5 or 3.0 mg/kg) dos e-dependently induced EEG desynchronization, as represented by a decre ase in root mean square (RMS) and an increase in mean power frequency (MPF) value of the EEG signals. Power spectral analysis further reveal ed that whereas both doses of cocaine promoted a reduction in the alph a (8-13 Hz), theta (4-8 Hz), and delta (1-4 Hz) components, the lower dose of cocaine decreased, and the higher dose increased the beta band (13-32 Hz). Microdialysis data indicated an elevation in extracellula r concentration of norepinephrine at the mPFC that paralleled temporal ly and correlated positively with the maximal effect of cocaine on EEG activity. Bilateral microinjection of the selective noradrenergic neu rotoxin, DSP4 (50 mu g), or equimolar concentration (500 pmol) of the alpha(1)-adrenoceptor antagonist, prazosin, or alpha(2)-adrenoceptor a ntagonist, yohimbine, into the mPFC significantly blunted the decrease in delta component (prazosin) or both delta and theta components (DSP 4 or yohimbine) of EEG activity by the lower dose of cocaine. On the o ther hand, the same pretreatments appreciably antagonized the increase in beta band by cocaine at 3.0 mg/kg. The potency of the antagonism b y yohimbine, however, was higher than prazosin. These results suggest that cocaine may elicit EEG desynchronization via noradrenergic neurot ransmission, and that alpha(2)-adrenoceptors, and to a lesser extent, alpha(1)-adrenoceptors, at the mPFC may be involved in the subtle dose -dependent changes in individual EEG spectral components. (C) 1995 Wil ey-Liss, Inc.