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The Journal of Neurophysiology Vol. 84 No. 5 November 2000, pp. 2699-2702
Copyright ©2000 by the American Physiological Society
RAPID COMMUNICATION
1Instituto de Ciencias Biomédicas, Programa de Fisiología y Biofísica, Facultad de Medicina, Universidad de Chile; and 2Departamento de Neurología y Neurocirugía, Hospital Clínico José Joaquín Aguirre, Universidad de Chile, Casilla 70005, Santiago, Chile
Ocampo-Garcés, Adrián,
Enrique Molina,
Alberto Rodríguez, and
Ennio A. Vivaldi.
Homeostasis of REM Sleep After Total and Selective Sleep
Deprivation in the Rat. J. Neurophysiol. 84: 2699-2702, 2000. During specific rapid eye movement (REM) sleep
deprivation its homeostatic regulation is expressed by progressively
more frequent attempts to enter REM and by a compensatory rebound after
the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be
differentially related to non-REM (NREM) and wakefulness. This problem
bears direct implications on the issue of the function of REM and its
relation to NREM. We compared three protocols that combined
REM-specific and total sleep deprivation so that animals underwent
similar 3-h REM deprivations but different concomitant NREM
deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours.
Deprivation periods started at hour 6 after lights on. Twenty-two
chronically implanted rats were recorded. The median amount of REM
during all three protocols was ~1 min. The deficits of median amount
of NREM in minutes within the 3-h deprivation periods as compared with
their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%),
25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding
hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among
protocols. Attempted transitions to REM showed a rising trend during
REM deprivations reaching a final value that did not differ
significantly among the three protocols. These results support the
hypothesis that the build up of REM pressure and its subsequent rebound
is primarily related to REM absence independent of the presence of NREM.
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