The control of posture and movements during REM sleep: neurophysiological and neurochemical mechanisms.
Mammalian sleep is characterized by synchronized sleep, in which high-amplitude, low-frequency waves appear in the electroencephalogram, and desynchronized sleep, characterized by small-amplitude, high-frequency waves, absence of tonic muscle activity, and rapid eye movements (REM), which are associated in humans with dreams. The postural atonia typical of desynchronized sleep is due to postsynaptic inhibition of spinal motoneurons resulting from tonic activation of a bulbospinal inhibitory system. Superimposed on this background of postural atonia, a motor pattern appears, characterized by rapid contractions of the limb musculature synchronous with the REM bursts. Simultaneously one observes phasic inhibition of transmission of somatic afferent volleys to motoneurons and ascending spinal pathways. The bursts of REM depend upon rhythmic discharges of vestibulo-oculomotor neurons, due to extralabyrinthine volleys originating from the brainstem. Ascending and descending vestibular volleys are also able to excite corticospinal and other supraspinal descending neurons responsible for the motor events synchronous with the bursts of REM. Activation of cholinergic neurons located in the brainstem reticular formation reproduces the postural atonia typical of desynchronized sleep, as well as the phasic events characterized by the REM bursts and the related changes in spinal cord activities. Even in this instance the bursts of REM and the related spinal effects depend upon rhythmic changes in the discharge of vestibular nuclear neurons. Experimental evidence indicates that the cholinergic reticular neurons fire asynchronously, thus being able to trigger the bulbospinal inhibitory system responsible for postural atonia. Even the vestibulo-oculomotor neurons are activated by these cholinergic reticular neurons; however, the continuous stream of these extralabyrinthine impulses is transformed into rhythmic changes of discharge of the vestibular nuclear neurons due to the presence of inhibitory neurons interposed with the vestibulo-oculomotor system. Waxing and waning in the activity of these cholinergic reticular neurons accounts for the regular occurrence of the cholinergically induced bursts of REM.
Pompeiano
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Institute of Physiology II, University of Pisa, Pisa, Italy.
D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000818:Animals; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology; D002415:Cats; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004569:Electroencephalography; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009068:Movement / Q000502:physiology*; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D010830:Physostigmine / Q000494:pharmacology; D011187:Posture / Q000502:physiology*; D012110:Reserpine / Q000494:pharmacology; D012895:Sleep, REM / Q000187:drug effects / Q000502:physiology*; D014726:Vestibular Nuclei / Q000187:drug effects / Q000502:physiology*; D014722:Vestibule, Labyrinth / Q000187:drug effects / Q000294:innervation / Q000502:physiology
D018759:Adrenergic Uptake Inhibitors; D002800:Cholinesterase Inhibitors; D012110:Reserpine; D010830:Physostigmine