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Sleep patterning and behaviour in cats with pontine lesions creating REM without atonia
Author(s) -
FORD LARRY D. SAN,
MORRISON ADRIAN R.,
MANN GRAZIELLA L.,
HARRIS JONATHAN S.,
YOO LAWRENCE,
ROSS RICHARD J.
Publication year - 1994
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.1994.tb00136.x
Subject(s) - tegmentum , rapid eye movement sleep , slow wave sleep , eye movement , brainstem , neuroscience , psychology , wakefulness , sleep (system call) , paramedian pontine reticular formation , circadian rhythm , pons , cats , tonic (physiology) , sleep spindle , non rapid eye movement sleep , midbrain , medicine , electroencephalography , reticular formation , stimulation , central nervous system , computer science , operating system
SUMMARY Lesions of the dorsal pontine tegmentum release muscle tone and motor behaviour, much of it similar to orienting during wakefulness, into rapid eye movement sleep (REM), a state normally characterized by paralysis. Sleep after pontine lesions may be altered, with more REM‐A episodes of shorter duration compared to normal REM. We examined behaviour, ponto‐geniculo‐occipital (PGO) waves (which may be central markers of orienting) and sleep in lesioned cats: (i) to characterize the relationship of PGO waves to behaviour in REM‐A; (ii) to determine whether post‐lesion changes in the timing and duration of REM‐A episodes were due to activity‐related awakenings; and (iii) to determine whether alterations in sleep changed the circadian sleep/wake cycle in cats. Behavioural release in REM‐A was generally related to episode length, but episode length was not necessarily shorter than normal REM in cats capable of full locomotion in REM‐A. PGO wave frequency was reduced overall during REM‐A, but was higher during REM‐A with behaviour than during quiet REM‐A without overt behaviour. Pontine lesions did not significantly alter the circadian sleep/wake cycle; REM‐A had approximately the same Light/Dark distribution as normal REM. Differences in the patterning of normal REM and REM‐A within sleep involve more than mere movement‐induced awakenings. Brainstem lesions that eliminate the atonia of REM may damage neural circuitry involved in REM initiation and maintenance; this circuitry is separate from circadian control mechanisms.