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Respiration et sommeil

Neurosciences
 
-La revue Neuroscience (2010 Sep 29;170(1):298-307. Epub 2010 Jul 8) publie une étude intitulée “Quinolinate induces selective loss of melanin-concentrating hormone neurons, rather than orexin neurons, in the hypothalamus of mice and young rats.” En observant la toxicité du quinolinate sur les neuropeptides hypocrétine et l'hormone concentrant la mélanine (HCM), cette étude vient bousculer l’hypothèse selon laquelle le mécanisme physiopathologique d’excitotoxicité provoqué par l’excitoxine N-methyl-D-aspartate (NMDA) serait un moment clé dans la pathogenèse de la narcolepsie.
 
Respiration
 
-Les agrégats de peptide bêta-amyloïde sont identifiés dans l'étiologie de la démence de type Alzheimer. Une étude parue dans la revue Brain Research explore quant à elle, sur des modèles animaux, le mécanisme induisant l’apparition de peptides bêta-amyloïde en contexte de syndrome d’apnées du sommeil chronique, neurotoxicité issue du phénomène d’hypoxie intermittente. Cette étude révèle également la pertinence thérapeutique de la mélatonine qui doit permettre la réduction de cette concentration de bêta-amyloïde dans l’hippocampe chez les patients porteurs d'un SAS chronique.
 
Psychiatrie
 
-La privation de sommeil est reconnue comme susceptible de réduire le symptôme dépressif sur 24 heures. Cependant, la nuit qui s’ensuit, une rechute des patients est le plus souvent observée. Il apparaît par ailleurs que même des micro-endormissements en période de privation de sommeil sont passibles d’entraîner une prompte rechute dans la dépression. Une étude parue dans le Journal of Psychiatric Research (2010 Oct;44(13):853-64. Epub 2010 Feb 19) est venue tester l’efficacité du modafinil sur ces micro-endormissements. Cette efficacité se voit confirmée sur les micro-endormissements le jour ayant suivi la privation de sommeil partielle, mais non pas lors de cette privation de sommeil, ni non plus en tant que facteur permettant la stabilisation des effets antidépresseurs de la privation de sommeil sur une plus longue période.
 
Sommeil et douleur
 
-Une étude parue dans la revue Pain (2010 Oct;151(1):220-5. Epub 2010 Aug 16) explore, à partir de la modélisation de données longitudinales  (témoignages subjectifs et actigraphie), les relations entre sommeil et douleur chez 39 adolescents souffrant de douleurs chroniques. Afin d'optimiser la caractérisation de ce phénomène,  ces données couplées, ainsi que des données relatives au genre, âge, existence d'antécédents dépressifs, ont été comparés aux données enregistrées chez 58 sujets sains. 
 

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Brain Res. 2010 Oct 1;1354:163-71. Epub 2010 Jul 21.
 
Melatonin reduces hippocampal beta-amyloid generation in rats exposed to chronic intermittent hypoxia.
Ng KM, Lau CF, Fung ML.
Research Centre of Heart, Brain, Hormone and Healthy Ageing, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong. skykmng@hkucc.hku.hk
Abstract
The deposition of neurotoxic beta-amyloid plaques plays a central role in the pathogenesis of Alzheimer's disease. At the molecular level, the generation of beta-amyloid peptides involves the site-specific cleavage of the precursor protein by beta-site APP cleavage enzyme (BACE) and presenilin. Although acute or chronic sustained hypoxia appears to increase the generation of beta-amyloid peptides via the HIF-1 alpha dependent upregulation of BACE, the effect of chronic intermittent hypoxia (CIH) on the generation of beta-amyloid peptides remains uncertain. In this study, we have evaluated such contention in the rat hippocampus, and we found that short-term CIH exposure (3 days) caused significant increases in the generation of beta-amyloid peptides, and the expressions of BACE, presenilin and HIF-1 alpha protein levels, in the hippocampus of CIH rats. Moreover, the CIH-induced hippocampal beta-amyloid peptide generation could be abolished by a daily pharmacological administration of melatonin (10mg/kg), which reduced the BACE but not presenilin expression. Also, there were no significant differences in the hippocampal HIF-1 alpha protein levels between the melatonin- and vehicle-treated CIH groups. Our study not only provided the first evidence that short-term CIH exposure could induce the beta-amyloid peptide generation in the hippocampus, but also pointed out the therapeutic value of melatonin in reducing beta-amyloid peptide generation in patients suffering from chronic obstructive sleep apnea syndrome.
PMID: 20654588 [PubMed - in process]
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J Psychiatr Res. 2010 Oct;44(13):853-64. Epub 2010 Feb 19.
Modafinil reduces microsleep during partial sleep deprivation in depressed patients.
Beck J, Hemmeter U, Brand S, Muheim F, Hatzinger M, Holsboer-Trachsler E.
Psychiatric Hospital of the University of Basel, Center of Affective Disorders and Depression and Center of Sleep Medicine, Basel/CH, Switzerland. johannes.beck@upkbs.ch
Abstract
OBJECTIVE: Sleep deprivation (SD) can induce a prompt decrease in depressive symptoms within 24h. Following the recovery night, however, a relapse into depression occurs in most patients. Recovery sleep, naps and even very short episodes of sleep (microsleep; MS) during SD have been shown to provoke a rapid relapse into depression. This study tested the hypothesis that modafinil reduces MS during SD and stabilizes the treatment response to PSD compared to placebo.
METHODS: A total of 28 patients (13 men, 15 women; age 45.1+/-12.1years) with a major depressive episode and a cumulative daytime microsleep of five or more minutes were investigated using a double-blind placebo-controlled study design. All patients were treated with a stable mirtazapine monotherapy. A partial SD (PSD) was performed after one week. Additional morning treatment with modafinil vs. placebo started during PSD and was maintained over two weeks. Sleep-EEG and MS episodes were recorded with a portable EEG. Depression severity was assessed using the Hamilton Depression Rating Scale before, during and after PSD and at follow-ups after one and two weeks.
RESULTS: Patients treated with modafinil showed significantly reduced microsleep during PSD (11.63+/-15.99min) compared to the placebo group (47.77+/-65.31min). This suppression of MS was not associated with the antidepressive effect of PSD.
CONCLUSIONS: Compared to placebo, modafinil was efficient in reducing daytime microsleep following partial sleep deprivation but did not enhance the antidepressive effects of PSD and did not stabilize antidepressive effects over two weeks.
PMID: 20171656 [PubMed - in process]
 
Pain. 2010 Oct;151(1):220-5. Epub 2010 Aug 16.
 
Temporal daily associations between pain and sleep in adolescents with chronic pain versus healthy adolescents.
Lewandowski AS, Palermo TM, Motte Sde L, Fu R.
Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA.
Abstract
Adolescents with chronic pain frequently report sleep disturbances, particularly short sleep duration, night wakings, and poor sleep quality. Prior research has been limited by assessment of subjectively reported sleep only and lack of data on daily relationships between sleep and pain. The current study utilized multilevel modeling to compare daily associations between sleep and pain in adolescents with chronic pain and healthy adolescents. Ninety-seven adolescents (n=39 chronic pain; n=58 healthy) aged 12-18, 70.1% female participated. Adolescents completed pain diary ratings (0-10 NRS) and actigraphic sleep monitoring for 10days. Actigraphic sleep variables (duration, efficiency, WASO) and self-reported sleep quality were tested as predictors of next-day pain, and daytime pain was tested as a predictor of sleep that night. Effects of age, gender, study group, and depressive symptoms on daily associations between sleep and pain were also tested. Multivariate analyses revealed that nighttime sleep (p<.001) and minutes awake after sleep onset (WASO) (p<.05) predicted next-day pain, with longer sleep duration and higher WASO associated with higher pain. Contrary to hypotheses, neither nighttime sleep quality nor sleep efficiency predicted pain the following day. The interaction between nighttime sleep efficiency and study group was significant, with adolescents with pain showing stronger associations between sleep efficiency and next-day pain than healthy participants (p=.05). Contrary to hypotheses, daytime pain did not predict nighttime sleep. Daily associations between pain and sleep suggest that further work is needed to identify specific adolescent sleep behaviors (e.g., compensatory sleep behaviors) that may be targeted in interventions.
PMID: 20719433 [PubMed - in process]
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Neuroscience. 2010 Sep 29;170(1):298-307. Epub 2010 Jul 8.
Quinolinate induces selective loss of melanin-concentrating hormone neurons, rather than orexin neurons, in the hypothalamus of mice and young rats.
Obukuro K, Takigawa M, Hisatsune A, Isohama Y, Katsuki H.
 
Department of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Abstract
Orexins are neuropeptides produced in the lateral hypothalamus and implicated in regulation of sleep-wake cycle. Selective loss of orexin neurons is found in the brain of patients with narcolepsy, but the mechanisms of this pathological change are unclear. A previous study showed that excessive stimulation of N-methyl-d-aspartate (NMDA) receptors by quinolinic acid (QA) caused selective loss of orexin neurons in rat hypothalamic slice culture. Here we examined QA toxicity on orexin neurons and melanin-concentrating hormone (MCH) neurons in vivo. Contrary to the expectation, injection of QA (60 and 120 nmol) into the lateral hypothalamus of male C57BL/6 mice caused selective loss of MCH neurons rather than orexin neurons, and this toxicity of QA was attenuated by MK-801, an NMDA receptor antagonist. Selective loss of MCH neurons with preserved orexin neurons was observed even when GABA(A) receptor antagonists such as bicuculline and picrotoxin were injected with QA. A significant decrease in the number of orexin neurons was induced when QA injection was performed in the dark phase of diurnal cycle, but the degree of the decrease was still lower than that in the number of MCH neurons. Finally, QA (60 nmol) induced selective loss of MCH neurons also in young rats at 3-4 weeks of age. These results do not support the hypothesis that acute excitotoxicity mediated by NMDA receptors is responsible for the pathogenesis of narcolepsy.
PMID: 20620197 [PubMed - in process]

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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.