REM-SLEEP INHIBITION BY DESIPRAMINE - EVIDENCE FOR AN ALPHA-1-ADRENERGIC MECHANISM

The acute administration of drugs that block norepinephrine (NE) reupt ake suppresses rapid eye movement (REM) sleep in cats and other mammal s. The mechanism is presumed to involve NE acting on cells in a pontin e REM sleep-generator region. Postsynaptic noradrenergic receptor mech anisms have not been identified. In the present experiments, we tested the ability of the alpha-1 antagonist prazosin and the beta antagonis t propranolol to reverse the REM sleep suppression produced by the NE reuptake blocker desipramine (DMI) in the cat. DMI reduced the number of REM sleep episodes, the REM percentage (REM sleep time/total sleep time), and the average REM sleep episode duration. The co-administrati on of prazosin, but not propranolol, increased the REM percentage and the average REM sleep episode duration toward the placebo level. The c o-administration of the peripherally-acting, anti-hypertensive agent h ydralazine did not reverse the DMI-induced REM sleep suppression. Whil e the identity of the brain region(s) involved in mediating the alpha- 1 noradrenergic suppression of REM sleep by DMI remains unclear, there is reason to consider forebrain structures including the amygdala as well as the pontine areas that generally have been implicated in REM s leep control.