Abstract
We hypothesize that rapid eye movements (REM) sleep may play a role in maintaining the functioning of catecholamine-containing neurons in the central nervous system. The main lines of evidence supporting this view are (a) following REM deprivation the responsiveness of catecholamine systems is depressed; (b) administration of drugs which enhance catecholamine activity can reverse some of the behavioral deficits which occur after REM deprivation; and (c) acute administration of pharmacological agents which depress catecholamine activity (alpha methyltyrosine, reserpine) produce a “compensatory≓ increase in REM time whereas increasing central catecholamine availability at the synapse (electroconvulsive shock, imipramine, monoamine oxidase inhibitors) decreases REM sleep. It is suggested that the mechanism of REM is primarily cholinergic and that the locus coeruleus may be the site of interaction between the catecholamine-REM function and the cholinergic-REM mechanism. Evidence is discussed relating to the possibility that REM sleep may have a more general function in the central nervous system, i.e., the modulation of protein synthesis in the brain.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call