Skip to main content Accessibility help
×
Home
  • Print publication year: 2011
  • Online publication date: September 2011

10 - Understanding REM sleep: clues from brain lesion studies

from Section III - Neuronal regulation

Summary

Summary

We have used the brain lesion method and chronically maintained cats to elucidate the contribution of key encephalic structures to the control of REM sleep. The results indicate that the physiological processes that participate in REM sleep generation and maintenance are all located in the pons, with the exception of those involved in REM sleep homeostasis. As we have shown, after a mesencephalic transection, REM sleep-deprived cats show a strong REM sleep pressure, but rebound does not occur. This finding indicates that the pontine mechanisms are modulated by a complex forebrain system, which, as we have shown, originates in the neocortex and has a powerful diencephalic stage. Part of this descending influence is a permissive mechanism for REM sleep rebound, which probably originates in the hypothalamus. Therefore the ultimate control of REM sleep rebound originates in the forebrain. This makes sense because it allows for a needed tight coupling with NREM sleep, which, as is well known, is also controlled by the forebrain. We have demonstrated that the electrocortical desynchronization induced by REM sleep is stronger that the one seen during waking (W), and this allows for REM sleep to accomplish what, we believe, is perhaps an REM sleep main function, i.e., to maintain the continuity of true sleep (S) given the limited duration of NREM sleep periods (by co-opting W at the end of NREM sleep periods).

Related content

Powered by UNSILO
Benington, J. H. & Heller, H.C. (1999) Implications of sleep deprivation experiments for our understanding of sleep homeostasis. Sleep 22: –37.
Berlucchi, G. . (1964) Pupil behavior and ocular movements during synchronized and desynchronized sleep. Arch Ital Biol 102: –44.
Bricolo, A. (1967) Insomnia after bilateral stereotactic thalamectomy in man. J Neurol 30: –8.
Carreras, M. . (1969) Residual neurons of the thalamic ventrobasal nuclei: a histological and electrophysiological study in the cat. Arch Ital Biol 107: –603.
de Andrés, I. . (1984) Reassessing morphine effects in cats: II. Protracted effects on sleep-wakefulness and the EEG. Pharmacol Biochem Behav 21: –8.
de Andrés, I. & Corpas, I. (1991) Morphine effects in brain stem-transected cats: II. Behavior and sleep of the decerebrate cat. Behav Brain Res 44: –6.
de Andrés, I. . (2003) The disconnected brain stem does not support rapid eye movement sleep rebound after selective deprivation. Sleep 26: 419–25.
Gong, , . (2004) Activation of CABAergic neurons in the preoptic area during sleep and in response to sleep deprivation. J Physiol 556: –46.
Guilleminault, C., Dement, W. C. & Passouant, P. eds. (1976) Narcolepsy: Advances in Sleep Research. New York:Spectrum.
Guilleminault, C. . eds. (1994) Fatal Familial Insomnia Inherited Prion Disease, Sleep, and the Thalamus. New York: Raven Press.
Hauri, P. & Hawkins, D. R. (1972) Human sleep after leucotomy. Arch Gen Psychiat 26: –73.
Heath, R. G. & Hodes, R. (1952) Induction of sleep by stimulation of the caudate nucleus in macacus rhesus and man. Trans Amer Neurol Assoc 77: –10.
Hernández-Peón, R. . (1967) Sleep and other behavioral effects induced by acetylcholine stimulation of the basal temporal cortex and striate structures. Brain Res 4: –67.
Hosokawa, K. J. . (1968) Follow-up studies on the sleep EEG after frontal lobotomy. Folia Psychit Neurol Jap 22: –43.
Jouvet, M. (1962) Recherches sur les structures nerveuses et les méchanismes responsables des différentes phases du sommeil physiologique. Arch Ital Biol 100: –206.
Jouvet, M. . (1961) Etudes polygraphiques des différent phases des sommeil au course des troubles de conscience chronique (commas prolongés). Rev Neurol 105: –6.
Kim, C. . (1975) Effects of hippocampectomy on sleep patterns in cats. Electroenceph Clin Neurophysiol 38: –43.
Kleitman, N. & Camille, N. (1932) Studies on the physiology of sleep. VI. The behavior of decorticate dogs. Am J Physiol 100: –80.
Lineberry, C. G. & Siegel, J. (1971) EEG synchronization, behavioral inhibition, and mesencephalic unit effects produced by stimulation of the orbital cortex, basal forebrain and caudate nucleus. Brain Res 34: –61.
Lu, J. . (2002) Selected activation of the extended ventrolateral preoptic nucleus during rapid eye movement sleep. J Neurosci 22: –76.
Lugaresi, E. . (1986) Fatal familial insomnia and dysautonomia with selective degeneration of thalamic nuclei. N Engl J Med 315: –1003.
McGinty, D. & Szymusiak, R. (2001) Brain structures and mechanisms involved in the generation of NREM sleep: focus on the preoptic hypothalamus. Sleep Res Rev 5: –42.
McGinty, D. & Szymusiak, R. (2003) Hypothalamic regulation of sleep and arousal. Front Biosci 8: –83.
Mittler, M. M. . (1974) Narcolepsy-cataplexy in a female dog. Exp Neurol 45: –40.
Naquet, R. . (1965) Altérations transitoires ou définitives des zones diencéphaliques chez le chat. Leurs effects sur l’activité corticales et le sommeil. In Aspect Anatomo-fonctionelle de la Physiologie du Sommeil, ed. Jouvet, M.. Paris: Editions de Centre Nationale de la Recherche Scientifique, pp. 107–31.
Passouant, P. & Cadilhac, J. (1962) Les rhythms theta hippocampiques au cours de sommeil. In Physiologie de l’hippocampe. ed. Passouant, P.. Paris: C. N. R. S., pp. 331–47.
Peñaloza-Rojas, . (1964) Sleep induced by cortical stimulation. Exp Neurol 10: –7.
Saper, C. B., Chou, T.C. & Scammel, T. E. (2001) The sleep switch: hypothalamic control of sleep and wakefulness. Trends Neurosci 24: –31.
Siegel, J. M. (2004) Hypocretin (Orexin): role in normal behavior and neuropathology. Ann Rev Psychol 55: –48.
Siegel, J. M. . (1986) Behavioral states in the chronic medullary and midpontine cat. Electroenceph Clin Neurophysiol 63: –88.
Villablanca, J. (1966) A behavioral and polygraphic study of “sleep” and “wakefulness” in chronic decerebrate cats. Electroenceph Clin Neurophysiol 21: –77.
Villablanca, J. R. (1994) Role of the diencephalon in sleep rebound. In Fatal Familial Insomnia: Inherited Prion Diseases, Sleep, and the Thalamus. eds. Guilleminault, C. . New York: Raven Press, pp. –59.
Villablanca, J. R. (2004) Counterpointing the functional role of the forebrain and of the brain stem in the control of the sleep-waking system. J Sleep Res 13: –298.
Villablanca, J. R. . (1976) Effects of caudate nuclei or frontal cortex ablations in cats. II. Sleep-wakefulness, EEG and motor activity. Exp Neurol 53: –50.
Villablanca, J. R. . (1984) Reassessing morphine effects in cats. I. Specific behavioral responses in intact and unilaterally brain-lesioned animals. Pharmacol Biochem Behav 21: –21.
Villablanca, J. R. . (2003) Debating how rapid eye movement sleep is regulated (and by what). J Sleep Res 12: –62.
Villablanca, J. & Marcus, R. J. (1972) Sleep-wakefulness, EEG and behavioral studies of chronic cats without neocortex and striatum: the 201C diencephalic 201D cat. Arch Ital Biol 110: –82.
Villablanca, J. & Salinas-Zeballos, M. E. (1972) Sleep-wakefulness, EEG and behavioral studies of chronic cats without the thalamus: the “athalamic” cat. Arch Ital Biol 110: –411.
Yamuy, J. . (2004) Hypocretinergic control of spinal cord motoneurons. J Neurosci 24: –45.
Zhang, J. X. . (1987) Abscence de rebound de sommeil paradoxale chez de rats hypophysectomisé et prétretés à la naissance par le glutamate de sodioum. C R Acad Sci 305: –8.