Experimental acceleration and slowing of REM sleep ultradian rhythm by cholinergic agonist and antagonist

It is demonstrated here that a normal 104-min REM sleep ultradian rhythm can be experimentally shortened to a 56-min rhythm by repeated infusions of arecholine, a cholinergic muscarinic agonist, and Conversely, scopolamines prolonged the interval between successive REM periods.

Abstract

MAMMALIAN sleep is characterised by the cyclical occurrence of rapid eye movement (REM) and non-REM sleep. In humans, REM sleep (consisting of a desyncronised electroencephalogram (EEG), rapid eye movements, atonic electromyogram (EMG), and usually accompanied by dreaming), occurs every 90–110 min1 and is presumed to be under the control of an underlying ultradian oscillatory mechanism2. The biological basis of the above ultradian rhythm is unknown. Although in humans the amount of REM sleep itself can be experimentally increased3–6 or decreased7–9 by pharmacological and physiological means, none of these manipulations has been shown to alter the frequency of its presumed oscillator. We demonstrate here that a normal 104-min REM sleep ultradian rhythm can be experimentally shortened to a 56-min rhythm by repeated infusions of arecholine, a cholinergic muscarinic agonist10. Conversely, scopolamine, a cholinergic muscarinic antagonist11, prolonged the interval between successive REM periods. We speculate that acetylcholine may have a specific role in the timing of the ultradian oscillatory mechanism controlling REM sleep.