We evaluated the effect and action mechanisms of cocaine on electroencephalographic (EEG) activity in adult male Sprague‐Dawley rats anesthetized with chloral hydrate (400 mg/kg, i.p., with 80 mg/kg/h supplements). On‐line and real‐time power spectral analysis of the EEG activity continuously quantified its root mean square (RMS) and mean power frequency (MPF) values, and the power of its spectral frequency components (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 desynchronization, as manifested by a reduction in RMS and an elevation in MPF values, coupled with a differential decrease in both high and low frequency components. Samples collected by in vivo microdialysis at the medial prefrontal cortex (mPFC) and analyzed by HPLC showed that the elevation of cocaine and dopamine (DA) level in the dialysate reached its peak during the time interval when maximal activation of EEG occurred. This EEG activation was antagonized by microinfusion into the mPFC via reverse microdialysis of R(+)‐SCH 23390, a selective antagonist for D‐1 receptors; sulpiride, a selective antagonist for D‐2 receptors; or haloperidol, a nonspecific dopamine antagonist. These results suggest that dopaminergic neurotran:3mission at the mPFC may be intimately related 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. © 1994 Wiley‐Liss, Inc.
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