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Morphine-induced activation of fetal EEG is mediated via central muscarinic pathways.

The effect of morphine on fetal electroencephalogram (EEG) was investigated using power spectral analysis. Morphine (0.15-5.0 mg/h) administered directly to the fetal lamb altered fetal EEG in three ways. First, morphine altered the relative incidence of the three preponderant EEG states [high-voltage slow activity (HVSA), transitional, and low-voltage fast activity (LVFA)]. Morphine resulted in a dose-dependent reduction in HVSA, with a reciprocal increase in transitional state at the lower doses and an increase in LVFA at higher doses. Second, morphine resulted in a more fragmented and unstable EEG pattern, with a significant increase in the number of state-to-state transitions. Third, there was a significant increase in the 90% spectral edge frequency as well as relative power distribution in the theta band. Taken together, these data suggest that morphine results in activation of the fetal EEG. This effect was completely abolished by concurrent intracerebroventricular administration of either methyl naloxone or methyl atropine, indicating that it is mediated by specific opioid receptors in the central nervous system and involves activation of central muscarinic pathways.