Neuroligin-1 links neuronal activity to sleep-wake regulation.

Détails

ID Serval
serval:BIB_FFF6E476695A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Neuroligin-1 links neuronal activity to sleep-wake regulation.
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur⸱e⸱s
El Helou J., Bélanger-Nelson E., Freyburger M., Dorsaz S., Curie T., La Spada F., Gaudreault P.O., Beaumont É., Pouliot P., Lesage F., Frank M.G., Franken P., Mongrain V.
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Statut éditorial
Publié
Date de publication
2013
Volume
110
Numéro
24
Pages
9974-9979
Langue
anglais
Résumé
Maintaining wakefulness is associated with a progressive increase in the need for sleep. This phenomenon has been linked to changes in synaptic function. The synaptic adhesion molecule Neuroligin-1 (NLG1) controls the activity and synaptic localization of N-methyl-d-aspartate receptors, which activity is impaired by prolonged wakefulness. We here highlight that this pathway may underlie both the adverse effects of sleep loss on cognition and the subsequent changes in cortical synchrony. We found that the expression of specific Nlg1 transcript variants is changed by sleep deprivation in three mouse strains. These observations were associated with strain-specific changes in synaptic NLG1 protein content. Importantly, we showed that Nlg1 knockout mice are not able to sustain wakefulness and spend more time in nonrapid eye movement sleep than wild-type mice. These changes occurred with modifications in waking quality as exemplified by low theta/alpha activity during wakefulness and poor preference for social novelty, as well as altered delta synchrony during sleep. Finally, we identified a transcriptional pathway that could underlie the sleep/wake-dependent changes in Nlg1 expression and that involves clock transcription factors. We thus suggest that NLG1 is an element that contributes to the coupling of neuronal activity to sleep/wake regulation.
Mots-clé
ChIP, EEG, gene expression, sleep homeostasis, synaptic plasticity
Pubmed
Web of science
Open Access
Oui
Création de la notice
14/08/2013 9:55
Dernière modification de la notice
20/08/2019 16:30
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