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

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 increased^3–6 or decreased^7–9 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.