Abstract

The serotonin-depleting drug, parachlorophenylalanine (PCPA), in a dosage of 300 mg/kg, was administered to rats in an effort to test the hypothesis that altered distribution of PGO waves following drug treatment may be responsible for the sleep disruption and consequent sleep loss that accompany decreased serotonin levels. Consistent with the hypothesis, we found that the greater the proportion of PGO waves that precede spontaneous arousals, the greater the reduction in slow wave sleep. However, inconsistent with the hypothesis, we found that the decrease in sleep did not result from an increase in the number of arousals. Further, though an increase in the proportion of waking waves always accompanied a rise in wake time, the two variables were negatively correlated. These data do not support a PGO wave/arousal hypothesis to account for the decrease in sleep following PCPA treatment in the rat. Rather, the findings tend to implicate an alteration in the mechanisms of arousal linked to serotonin depletion.

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