Dissociation of rapid eye movement (REM) sleep features: possible implications for REM triggering mechanisms.

Abstract

Neurophysiological and biochemical mechanisms regulating REM sleep episodes were studied in behaving cats with chronic electrodes. Push-pull perfusion of the midbrain or pontine reticular formation (RF) by a protein synthesis inhibitor, chloramphenicol (CAP), reduced neuronal unit discharge, particularly discharge bursts, within the perfused area, and reduced the incidence of sustained REM periods. During transitions to "aborted" as compared to sustained REM episodes. RF unit discharge was reduced, under all conditions. In 72-hour sleep deprived cats, systemic injections of both atropine (ATR) and CAP attenuated REM rebound, but with different patterns. CAP reduced REM episode frequency. ATR reduced REM duration. ATR also reduced PGO wave frequency. Combined CAP and ATR treatment produced additive REM depressant effects. These data suggest that cholinergic mechanisms regulate PGO activity and maintenance of REM episodes and that protein synthesis-dependent mechanisms regulate RF unit discharge bursts, and REM triggering.