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Titolo:
Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep(PS) propensity: evidence from a short-term PS deprivation study in rats
Autore:
Deurveilher, S; Hennevin, E;
Indirizzi:
Univ Paris Sud, Lab Neurobiol Apprentissage Memoire & Commun, CNRS, UMR 8620, F-91405 Orsay, France Univ Paris Sud Orsay France F-91405 NRS, UMR 8620, F-91405 Orsay, France
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 10, volume: 13, anno: 2001,
pagine: 1963 - 1976
SICI:
0953-816X(200105)13:10<1963:LOTPTN>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
PONTINE RETICULAR-FORMATION; EYE-MOVEMENT SLEEP; FREELY MOVING CATS; REM-SLEEP; BRAIN-STEM; CHOLINERGIC NEURONS; PONTOMESENCEPHALIC TEGMENTUM; ELECTRICAL-STIMULATION; MESOPONTINE TEGMENTUM; ACETYLCHOLINE-RELEASE;
Keywords:
ibotenate; PS attempts; PS rebound; REM sleep; sleep-waking states;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Hennevin, E Univ Paris Sud, Lab Neurobiol Apprentissage Memoire & Commun, CNRS, UMR 8620, F-91405 Orsay, France Univ Paris Sud Orsay France F-914050, F-91405 Orsay, France
Citazione:
S. Deurveilher e E. Hennevin, "Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep(PS) propensity: evidence from a short-term PS deprivation study in rats", EUR J NEURO, 13(10), 2001, pp. 1963-1976

Abstract

Cholinergic neurons in the mesopontine tegmentum are thought to play a critical role in the generation of paradoxical sleep (PS). However, no study has yet examined whether lesions of these neurons cause deficits of PS in the rat. We describe here the effects of lesions of the pedunculopontine tegmental nucleus (PPT) on spontaneous PS and on PS propensity, expressed during and after a short period of PS deprivation. Lesions were induced by bilateral injections of ibotenate. PS deprivation was performed manually by gently waking rats each time they showed polygraphic signs of PS. Two weeks after lesions, an 8-h baseline recording was performed; the following day, rats were PS deprived for 6 h and polygraphic recordings were then continued for 2 h, to examine recovery sleep. The same protocol was repeated 1 week later. Compared with controls and with rats with limited PPT lesions, rats bearing > 60% NADPH-diaphorase-positive cell loss within the PPT showed unaffected PS under baseline conditions. However, they made fewer attempts to enter PS during deprivation and they exhibited an attenuated rebound increasein PS time after deprivation. The number of PS attempts and the magnitude of PS rebound were negatively correlated with the percent loss of diaphorase-positive neurons within the PPT. Thus, PS propensity that accumulated as a result of PS deprivation was reduced after extensive PPT lesions. In summary, although spontaneous PS was found to be unaltered, the PS deprivation procedure used in this study demonstrated the dysfunctioning of PS caused by PPT lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 05:32:29