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

We evaluated the effect and action mechanisms of cocaine on electroenc ephalographic (EEG) activity in adult male Sprague-Dawley rats anesthe tized with chloral hydrate (400 mg/kg, i.p., with 80 mg/kg/h supplemen ts). On-line and real-time power spectral analysis of the EEG activity continuously quantified its root mean square (RMS) and mean power fre quency (MPF) values, and the power of its spectral frequency component s (low frequency: 0-4 Hz; high frequency: 4-20 Hz). Administration of cocaine (1.5 or 3.0 mg/kg, i.v.) dose-dependently induced EEG desynchr onization, as manifested by a reduction in RMS and an elevation in MPF values, coupled with a differential decrease in both high and low fre quency components. Samples collected by in vivo microdialysis at the m edial prefrontal cortex (mPFC) and analyzed by HPLC showed that the el evation of cocaine and dopamine (DA) level in the dialysate reached it s peak during the time interval when maximal activation of EEG occurre d. This EEG activation was antagonized by microinfusion into the mPFC via reverse microdialysis of R(+)-SCH 23390, a selective antagonist fo r D-1 receptors; sulpiride, a selective antagonist for D-2 receptors; or haloperidol, a nonspecific dopamine antagonist. These results sugge st that dopaminergic neurotransmission at the mPFC may be intimately r elated to the specific spectral pattern of alteration in EEG activity elicited by cocaine in the rat and that both D-1 and D-2 receptors may be involved in the process. (C) 1994 Wiley-Liss, Inc.