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régulation des émotions et cognition / Durée du sommeil et risques cardiovaculaires et métaboliques / Cannabinoïdes et système circadien

Santé publique
Ainsi une étude à paraître dans la revue Social Science and Medicine (2010 Sep;71(5):1027-36) met en évidence une association entre un temps de sommeil trop court < 7 heures ou un temps de sommeil « trop long » > 8 heures et le risque d’obésité, de risques cardiovasculaires, de diabète et d’hypertension. L’étude a porté sur les 56507 observations issues des données de la National Health Interview Survey 2004-2005 auprès d’adultes entre 18 et 85 ans. Les résultats ont été obtenus à partir d’une analyse de régression multivariée contrôlée par la prise en compte des données d’âge, de genre, d’appartenances ethniques et d’environnement social de ces individus. Parmi ces variables, la durée de sommeil s’est imposée comme la plus fortement corrélée à ces troubles cardiovasculaires et métaboliques.
Chronobiologie
Le Journal of  Neuroscience (28 Juillet, 2010, 30(30):10061-10066) examine les effets des cannabinoïdes sur le système circadien. La perte de repère temporel ressentie par les usagers de substances stupéfiantes étant susceptible de trouver une explication dans l’excitation engendrée par les cannabinoïdes sur les neurones de l’horloge circadienne.
Neurologie
La revue Current Biology 2010 10 août;20(15) publie une étude qui semble conforter l’hypothèse du rôle des fuseaux de sommeil (spindles) _ rythmes thalamo-corticaux spontanés perçus comme capables de moduler l’incidence des stimuli externes _ dans le maintien du sommeil.  Le protocole expérimental consistant en la lecture de l’activité cérébrale de 12 sujets sains dans les conditions d’une nuit normale et d’une nuit parasitée par des bruits a révélé que les sujets ayant généré plus de fuseaux de sommeil dans des conditions de sommeil normales ont su manifester une plus grande tolérance à un environnement de sommeil grevé de nuisances sonores.
Les effets du modafinil sur les circuits neuraux impliqués dans la régulation des émotions et le fonctionnement cognitif sont mis en évidence dans la revue Neuropsychopharmacology (2010) 35, 2101–2109). Il apparaît que le modafinil, plus que toute autre substance  stimulante, améliore la circulation de l’information dans la région du cortex préfrontal tout en tempérant la réactivité aux stimuli menaçants dans le complexe amygdalien, région du cerveau impliquée notamment dans le phénomène d’anxiété.


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Social Science and Medicine 2010 Sep;71(5):1027-36. Epub 2010 Jun 16.
Short and long sleep are positively associated with obesity, diabetes, hypertension, and cardiovascular disease among adults in the United States.
Buxton OM, Marcelli E.
Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Division of Sleep Medicine, BLI-438, 221 Longwood Avenue, Boston, MA 02115, United States. orfeu_buxton@hms.harvard.edu
Abstract
Research associates short (and to a lesser extent long) sleep duration with obesity, diabetes, and cardiovascular disease; and although 7-8 h of sleep seems to confer the least health risk, these findings are often based on non-representative data. We hypothesize that short sleep (<7 h) and long sleep (>8 h) are positively associated with the risk of obesity, diabetes, hypertension, and cardiovascular disease; and analyze 2004-2005 US National Health Interview Survey data (n=56,507 observations, adults 18-85) to test this. We employ multilevel logistic regression, simultaneously controlling for individual characteristics (e.g., ethnoracial group, gender, age, education), other health behaviors (e.g., exercise, smoking), family environment (e.g., income, size, education) and geographic context (e.g., census region). Our model correctly classified at least 76% of adults on each of the outcomes studied, and sleep duration was frequently more strongly associated with these health risks than other covariates. These findings suggest a 7-8 h sleep duration directly and indirectly reduces chronic disease risk. Copyright (c) 2010 Elsevier Ltd. All rights reserved.
PMID: 20621406 [PubMed - in process]
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The Journal of Neuroscience, July 28, 2010, 30(30):10061-10066; doi:10.1523/JNEUROSCI.5838-09.2010
Cannabinoids Excite Circadian Clock Neurons
Claudio Acuna-Goycolea,1 Karl Obrietan,2 and Anthony N. van den Pol1
1Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520, and 2Department of Neurobiology, Ohio State University, Columbus, Ohio 43210
Correspondence should be addressed to Anthony N. van den Pol, Department of Neurosurgery, Yale University, New Haven, CT 06520. Email: anthony.vandenpol@yale.edu
Cannabinoids, the primary active agent in drugs of abuse such as marijuana and hashish, tend to generate a distorted sense of time. Here we study the effect of cannabinoids on the brain's circadian clock, the suprachiasmatic nucleus (SCN), using patch clamp and cell-attached electrophysiological recordings, RT-PCR, immunocytochemistry, and behavioral analysis. The SCN showed strong expression of the cannabinoid receptor CB1R, as detected with RT-PCR. SCN neurons, including those using GABA as a transmitter, and axons within the SCN, expressed CB1R immunoreactivity. Behaviorally, cannabinoids did not alter the endogenous free-running circadian rhythm in the mouse brain, but did attenuate the ability of the circadian clock to entrain to light zeitgebers. In the absence of light, infusion of the CB1R antagonist AM251 caused a modest phase shift, suggesting endocannabinoid modulation of clock timing. Interestingly, cannabinoids had no effect on glutamate release from the retinohypothalamic projection, suggesting a direct action of cannabinoids on the retinohypothalamic tract was unlikely to explain the inhibition of the phase shift. Within the SCN, cannabinoids were excitatory by a mechanism based on presynaptic CB1R attenuation of axonal GABA release. These data raise the possibility that the time dissociation described by cannabinoid users may result in part from altered circadian clock function and/or entrainment to environmental time cues.
Received Nov. 23, 2009; revised June 10, 2010; accepted June 17, 2010.
Correspondence should be addressed to Anthony N. van den Pol, Department of Neurosurgery, Yale University, New Haven, CT 06520. Email: anthony.vandenpol@yale.edu
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Current Biology 2010 Aug 10;20(15):R626-R627.
Spontaneous brain rhythms predict sleep stability in the face of noise.
Dang-Vu TT, McKinney SM, Buxton OM, Solet JM, Ellenbogen JM.
Division of Sleep Medicine, Harvard Medical School, Boston, MA 02115, USA; Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Cyclotron Research Centre, University of Liege, Belgium.
Abstract
Quality sleep is an essential part of health and well-being. Yet fractured sleep is disturbingly prevalent in our society, partly due to insults from a variety of noises [1]. Common experience suggests that this fragility of sleep is highly variable between people, but it is unclear what mechanisms drive these differences. Here we show that it is possible to predict an individual's ability to maintain sleep in the face of sound using spontaneous brain rhythms from electroencephalography (EEG). The sleep spindle is a thalamocortical rhythm manifested on the EEG as a brief 11-15 Hz oscillation and is thought to be capable of modulating the influence of external stimuli [2]. Its rate of occurrence, while variable across people, is stable across nights [3]. We found that individuals who generated more sleep spindles during a quiet night of sleep went on to exhibit higher tolerance for noise during a subsequent, noisy night of sleep. This result shows that the sleeping brain's spontaneous activity heralds individual resilience to disruptive stimuli. Our finding sets the stage for future studies that attempt to augment spindle production to enhance sleep continuity when confronted with noise. Copyright © 2010 Elsevier Ltd. All rights reserved.
PMID: 20692606 [PubMed - as supplied by publisher]
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Neuropsychopharmacology (2010) 35, 2101–2109; doi:10.1038/npp.2010.83; published online 16 June 2010
Modulatory Effects of Modafinil on Neural Circuits Regulating Emotion and Cognition
Roberta Rasetti1,2, Venkata S Mattay1,2, Beth Stankevich1, Kelsey Skjei1, Giuseppe Blasi1,3, Fabio Sambataro1,4, Isabel C Arrillaga-Romany1, Terry E Goldberg1,5, Joseph H Callicott1, José A Apud1 and Daniel R Weinberger1
1Clinical Brain Disorders Branch: Genes, Cognition, and Psychosis Program, NIMH, NIH, Bethesda, MD, USA
Correspondence: Dr DR Weinberger, Genes, Cognition and Psychosis Program, IRP, NIMH, NIH, Rm. 4S-235, 10 Center Drive—Bethesda, MD 20892, USA, Tel: +301 402 7564, Fax: 301 480 7795, E-mail: daniel.weinberger@mail.nih.gov
2These authors contributed equally to this work.
3Current address: Department of Neurological and Psychiatric Sciences, Psychiatric Neuroscience Group, University of Bari, Bari, Italy
4Current address: Brain Center of Motor and Social Cognition, Italian Institute of Technology, Parma, Italy
5Current address: Long Island Jewish Medical Center, The Zucker Hillside Hospital, Glen Oaks, New York, USA
Received 25 February 2010; Revised 15 April 2010; Accepted 1 May 2010; Published online 16 June 2010.
Modafinil differs from other arousal-enhancing agents in chemical structure, neurochemical profile, and behavioral effects. Most functional neuroimaging studies to date examined the effect of modafinil only on information processing underlying executive cognition, but cognitive enhancers in general have been shown to have pronounced effects on emotional behavior, too. We examined the effect of modafinil on neural circuits underlying affective processing and cognitive functions. Healthy volunteers were enrolled in this double-blinded placebo-controlled trial (100 mg/day for 7 days). They underwent BOLD fMRI while performing an emotion information-processing task that activates the amygdala and two prefrontally dependent cognitive tasks—a working memory (WM) task and a variable attentional control (VAC) task. A clinical assessment that included measurement of blood pressure, heart rate, the Hamilton anxiety scale, and the profile of mood state (POMS) questionnaire was also performed on each test day. BOLD fMRI revealed significantly decreased amygdala reactivity to fearful stimuli on modafinil compared with the placebo condition. During executive cognition tasks, a WM task and a VAC task, modafinil reduced BOLD signal in the prefrontal cortex and anterior cingulate. Although not statistically significant, there were trends for reduced anxiety, for decreased fatigue-inertia and increased vigor-activity, as well as decreased anger-hostility on modafinil. Modafinil in low doses has a unique physiologic profile compared with stimulant drugs: it enhances the efficiency of prefrontal cortical cognitive information processing, while dampening reactivity to threatening stimuli in the amygdala, a brain region implicated in anxiety.
Keywords: modafinil; fMRI; emotion; amygdala; cognitive processing; healthy volunteers

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Groupe Santé Sommeil

Le groupe médical Santé Sommeil a pour vocation de diagnostiquer et traiter les troubles du sommeil et de la veille chez l’adulte et l’enfant.