Valérie Mongrain Professeure au Département de neurosciences de la Faculté de médecine, Valérie Mongrain obtient la Chaire de recherche du Canada en physiologie moléculaire du sommeil (niveau 2). Les répercussions du manque de sommeil chez les gens malades et les personnes en santé restent peu connues. Valérie Mongrain travaillera à désigner des molécules responsables des effets négatifs du manque de sommeil sur les fonctions neuronales afin de mieux comprendre comment le phénomène agit sur la santé mentale et la cognition. Investissement majeur pour la recherche à l’Université de Montréal | UdeMNouvellesPosted: December 20, 2016
Dix-huit chaires de recherche du Canada seront créées ou renouvelées à l’Université de Montréal.
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Gosselin et al (2016): BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative MemoriesPosted: December 19, 2016
It is hypothesized that a fundamental function of sleep is to restore an individual’s day-to-day ability to learn and to constantly adapt to a changing environment through brain plasticity. Brain-derived neurotrophic factor (BDNF) isamongthe key regulators that shape brain plasticity. However, advancing age and carrying the BDNF Met allele were both identified as factors that potentially reduce BDNF secretion, brain plasticity, and memory. Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years of age. All subjects were tested with 1 night of in-laboratory polysomnography followed by a cognitive evaluation the next morning. We found that in subjects carrying the BDNF Val66Val polymorphism, consolidated sleep was associated with significantly better performance on hippocampus-dependent episodic memory tasks the next morning (-values from 0.290 to 0.434, p0.01). In subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated with better memory performance in most memory tests (-values from0.309 to0.392, p values from 0.06 to 0.15). Strikingly, increased sleep consolidation was associated with poorer performance in learning a short story presented verbally in Met allele carriers (0.585, p 0.005). This study provides new evidence regarding the interacting roles of consolidated sleep andBDNFpolymorphism in the ability to learn and stresses the importance of consideringBDNFpolymorphism when studying how sleep affects cognition.
Nadia Gosselin, Louis De Beaumont, Katia Gagnon, Andree-Ann Baril, Valerie Mongrain, Helene Blais, Jacques Montplaisir, Jean-Francois Gagnon, Sandra Pelleieux, Judes Poirier, and Julie Carrier; The Journal of Neuroscience, August 10, 2016 • 36(32):8390–8398
Freyburger, et al (2016): phA4 is involved in sleep regulation but not in the electrophysiological response to sleep deprivationPosted: December 19, 2016
Study Objectives: Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements.
Methods: EphA4 knockout (KO) mice, ClockΔ19/Δ19 mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day.
Results: EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice.
Conclusions: Our results suggest that EphA4 is involved in circadian sleep regulation.
Citation: Freyburger M, Pierre A, Paquette G, Bélanger-Nelson E, Bedont J, Gaudreault PO, Drolet G, Laforest S, Blackshaw S, Cermakian N, Doucet G, Mongrain V. EphA4 is involved in sleep regulation but not in the electrophysiological response to sleep deprivation. SLEEP 2016;39(3):613–624.