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  Dissecting and modeling photic and melanopsin effects to predict sleep disturbances induced by irregular light exposure in mice

Hubbard, J., Kobayashi Frisk, M., Ruppert, E., Tsai, J. W., Fuchs, F., Robin-Choteau, L., et al. (2021). Dissecting and modeling photic and melanopsin effects to predict sleep disturbances induced by irregular light exposure in mice. Preoceedings of the National Academy of Sciences of the USA, 118(25): e2017364118. doi:10.1073/pnas.2017364118.

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Hubbard, J., Author
Kobayashi Frisk, M., Author
Ruppert, E., Author
Tsai, J. W., Author
Fuchs, F., Author
Robin-Choteau, L., Author
Husse, J., Author
Husse, J. L.1, Author              
Calvel, L., Author
Eichele, G.2, Author              
Franken, P., Author
Bourgin, P., Author
Affiliations:
1Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society, ou_persistent34              
2Emeritus Group of Genes and Behavior, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society, ou_3350144              

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Free keywords: circadian and noncircadia; nsleep–wake cycle; phototransduction; melanopsin; photoperiods
 Abstract: Artificial lighting, day-length changes, shift work, and transmeridian travel all lead to sleep–wake disturbances. The nychthemeral sleep–wake cycle (SWc) is known to be controlled by output from the central circadian clock in the suprachiasmatic nuclei (SCN), which is entrained to the light–dark cycle. Additionally, via intrinsically photosensitive retinal ganglion cells containing the photopigment melanopsin (Opn4), short-term light–dark alternations exert direct and acute influences on sleep and waking. However, the extent to which longer exposures typically experienced across the 24-h day exert such an effect has never been clarified or quantified, as disentangling sustained direct light effects (SDLE) from circadian effects is difficult. Recording sleep in mice lacking a circadian pacemaker, either through transgenesis (Syt10cre/creBmal1fl/-) or SCN lesioning and/or melanopsin-based phototransduction (Opn4−/−), we uncovered, contrary to prevailing assumptions, that the contribution of SDLE is as important as circadian-driven input in determining SWc amplitude. Specifically, SDLE were primarily mediated (>80%) through melanopsin, of which half were then relayed through the SCN, revealing an ancillary purpose for this structure, independent of its clock function in organizing SWc. Based on these findings, we designed a model to estimate the effect of atypical light–dark cycles on SWc. This model predicted SWc amplitude in mice exposed to simulated transequatorial or transmeridian paradigms. Taken together, we demonstrate this SDLE is a crucial mechanism influencing behavior on par with the circadian system. In a broader context, these findings mandate considering SDLE, in addition to circadian drive, for coping with health consequences of atypical light exposure in our society.

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Language(s): eng - English
 Dates: 2021-06-212021-06-22
 Publication Status: Published in print
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1073/pnas.2017364118
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Title: Preoceedings of the National Academy of Sciences of the USA
Source Genre: Journal
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Pages: 9 Volume / Issue: 118 (25) Sequence Number: e2017364118 Start / End Page: - Identifier: -