DIFFERENTIAL-EFFECTS OF CHLORAL HYDRATE AND PENTOBARBITAL SODIUM ON COCAINE-INDUCED ELECTROENCEPHALOGRAPHIC DESYNCHRONIZATION AT THE MEDIALPREFRONTAL CORTEX IN RATS

We evaluated the effects of two anesthetics on the cocaine-induced ele ctroencephalographic (EEG) desynchronization in male, Sprague-Dawley r ats. One group was anesthetized with chloral hydrate (400 mg/kg, i.p., 80 mg/kg/h i.v. supplement; group A). The other group was anesthetize d with pentobarbital sodium (50 mg/kg, i.p., 10 mg/kg/h i.v. supplemen t; group B). The degree of EEG desynchronization after cocaine adminis tration (1.5 mg/kg, i.v.) was expressed as an increase in the mean pow er frequency (MPF) and a decrease in the root mean square (RMS). These maximal increases and decreases were observed to be large in group A (MPF: 43.3 +/- 7.0% increase; RMS: 47.4 +/- 5.0% decrease) than in gro up B (MPF: 17.8 +/- 3.6% increase; RMS: 19.2 +/- 2.5% decrease). Our l aboratory previously proved that dopaminergic neurotransmission at the medial prefrontal cortex (mPFC) participated in the cocaine-induced E EG desynchronization and that both D-1 and D-2 receptors were involved in the process. Therefore, in vivo microdialysis coupled with high pe rformance liquid chromatography was used to quantify the changes of ex tracellular dopamine (DA) concentrations at the mPFC for 90 minutes at 10 minute intervals after 1.5 mg/kg cocaine i.v. injection. The extra cellular DA increases in both groups ws rapid and reached the maximal peak within 10 min. There was no significant difference in the maximal increase of DA between groups (group A: 375.2 +/- 35.77% versus group B: 332.2 +/- 16.69% over basal value). These results suggest that dif ferent anesthetics may differentially affect cocaine-induced EEG desyn chronization and this difference has no bearing on the DA response in the mPFC.