Effects of morphine on EEG in rats and their possible relations to hypo- and hyperkinesia

It was previously shown in rats that administration of cocaine ord-amphetamine in moderate doses produced alterations in EEG characteristic for activation of D₁ dopamine receptors, whereas large doses induced alterations resembling activation of D₂ dopamine receptors. Since morphine, among other effects, enhances the dopaminergic transmission, it was investigated whether this effect might be apparent in the EEG which was recorded telemetrically in awake, not restrained rats. In a moderate dose (3 mg/kg IP), morphine produced a desynchronisation and a general decrease of power in all of the frequency bands except beta-2. This effect was antagonized by naloxone (0.5 mg/kg IP) but only in part by the blocker of D₁ receptors SCH 23390 (0.2 mg/kg IP) and not by haloperidol in a dose which mainly blocks D₂ receptors (0.1 mg/kg IP). The dose of morphine used (3 mg/kg IP) produced only slight signs of behavioural activation. The results suggest that the decrease in power observed after this dose of morphine was only in part due to an activation of dopaminergic mechanisms via D₁ receptors and partly must be explained by other actions of morphine. A large dose of morphine (15 mg/kg IP) at the beginning produced catalepsy and muscular rigidity and subsequent behavioural activation; in the EEG during both behavioural phases a general increase in power in all of the frequency bands was observed which was most pronounced in the alpha-2 band (9.75–12.50 Hz). After repeated administration of this dose (14 times during a period of 21 days) a test dose of 15 mg/kg morphine led to a reversal of these effects resulting in behavioural activation and a decrease in power in most of the frequency bands. Accordingly, most but not all experimental conditions used led to consistent correlations between behavioural signs and EEG alterations after administration of morphine.