Abstract

In order to examine the prosencephalic mechanisms that might sustain the effects of opiates on EEG and sleep-wakefulness, the actions of morphine sulfate on the EEG and the pupil size were examined in the chronically isolated forebrain of brainstem-transected cats. Single morphine doses (0.5, 2.0 or 3.0 mg/kg, i.p.) administered to these animals produced a long-lasting EEG desynchronization in the isolated forebrain which was associated with pupil mydriasis. The specificity of these morphine effects was shown by the fact that naloxone blocks both the EEG and pupillary effects of the drug. After morphine, spontaneous synchronized EEG with delta waves normally seen in the isolated forebrain preparation was suppressed for 6-18 h, followed by a strong rebound. Both the suppression and rebound in synchronization with delta waves occurred in a dose-dependent manner. The duration of these effects closely paralleled previously reported morphine effects on non-rapid eye movement (NREM) sleep in intact cats. Therefore, in relation to the effects of morphine on EEG and sleep-wakefulness in intact animals, this study suggests that: (1) Morphine suppression of NREM sleep and the subsequent arousal state of the animal are mediated by prosencephalic structures; (2) the generation of the typical neocortical EEG slow burst activity produced by opiates depends on lower brainstem structures.