Cats receiving 0.15 mg/kg of reserpine, i.p., had rapid eye movement (REM) sleep suppressed for two days and showed increased ponto-geniculo-occipital (PGO) spikes in waking and slow-wave sleep; these effects were not reversed by administration of dopa. Reserpine (0.125 mg) given intraventricularly, however, significantly increased REM sleep and did not change the frequency of PGO spikes in waking and slow-wave sleep. The differences in sleep characteristics seen between i.p. and central administration of reserpine are probably due to (a) the marked peripheral autonomic side effects accompanying reserpine, i.p., and (b) the much smaller central depletion of brain monoamines following intraventricular reserpine. Also, the correspondance between the regional levels of brain biogenic amines and the occurrence of the sleep states is poor since REM and slow-wave were normal on the third day after reserpine, i.p., while norepinephrine and serotonin levels were depressed by about 50% at that time.
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