Neuronal mechanisms of respiration in REM sleep

Abstract

The irregular breathing charcteristic of rapid eye movement (REM) sleep does not result from variations in chemoreceptor (Guazzi and Freis, 1969) or vagal (Dawes et al., 1972; Remmers et al., 1976; Netick et al., 1977) or thoracic (Netick et al., 1977) afferent activity. It seems instead to be controlled by REM sleep processes (Orem, 1980). This was first proposed by several researchers shortly after REM sleep as a unique state was discovered, and it was suggested again recently when interest in breathing in sleep resurged in the wake of the recognition of the sleep apnea syndromes (Orem and Dement, 1976; Phillipson, 1978). The association of irregular breathing with the REM sleep process rather than metabolic or reflexive respiratory controllers was based on observations that irregular breathing tended to coincide with rapid eye movement bursts and other phasic REM sleep phenomena. Reports of this association were anecdotal and sometimes contradictory. Some authors reported that rapid eye movements were associated with hypopneas; others stated that they were associated with hyperpnea.