Rai1 frees mice from the repression of active wake behaviors by light.

Détails

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Etat: Serval
Version: Final published version
ID Serval
serval:BIB_2A7CEC2344D6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Rai1 frees mice from the repression of active wake behaviors by light.
Périodique
eLife
Auteur(s)
Diessler S., Kostic C., Arsenijevic Y., Kawasaki A., Franken P.
ISSN
2050-084X (Electronic)
ISSN-L
2050-084X
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
6
Pages
e23292
Langue
anglais
Résumé
Besides its role in vision, light impacts physiology and behavior through circadian and direct (aka 'masking') mechanisms. In Smith-Magenis syndrome (SMS), the dysregulation of both sleep-wake behavior and melatonin production strongly suggests impaired non-visual light perception. We discovered that mice haploinsufficient for the SMS causal gene, Retinoic acid induced-1 (Rai1), were hypersensitive to light such that light eliminated alert and active-wake behaviors, while leaving time-spent-awake unaffected. Moreover, variables pertaining to circadian rhythm entrainment were activated more strongly by light. At the input level, the activation of rod/cone and suprachiasmatic nuclei (SCN) by light was paradoxically greatly reduced, while the downstream activation of the ventral-subparaventricular zone (vSPVZ) was increased. The vSPVZ integrates retinal and SCN input and, when activated, suppresses locomotor activity, consistent with the behavioral hypersensitivity to light we observed. Our results implicate Rai1 as a novel and central player in processing non-visual light information, from input to behavioral output.

Mots-clé
circadian rhythm, human biology, light, medicine, mouse, neuroscience, sleep, smith-magenis syndrome, supra-chiasmatic nuclei, ventral-subparaventricular zone
Pubmed
Web of science
Création de la notice
06/06/2017 20:28
Dernière modification de la notice
03/03/2018 15:23
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