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   Melanopsin Regulates Both Sleep-Promoting and Arousal-Promoting Responses to Light  
   
نویسنده pilorz v. ,tam s.k.e. ,hughes s. ,pothecary c.a. ,jagannath a. ,hankins m.w. ,bannerman d.m. ,lightman s.l. ,vyazovskiy v.v. ,nolan p.m. ,foster r.g. ,peirson s.n.
منبع plos biology - 2016 - دوره : 14 - شماره : 6
چکیده    Light plays a critical role in the regulation of numerous aspects of physiology and behaviour,including the entrainment of circadian rhythms and the regulation of sleep. these responses involve melanopsin (opn4)-expressing photosensitive retinal ganglion cells (prgcs) in addition to rods and cones. nocturnal light exposure in rodents has been shown to result in rapid sleep induction,in which melanopsin plays a key role. however,studies have also shown that light exposure can result in elevated corticosterone,a response that is not compatible with sleep. to investigate these contradictory findings and to dissect the relative contribution of prgcs and rods/cones,we assessed the effects of light of different wavelengths on behaviourally defined sleep. here,we show that blue light (470 nm) causes behavioural arousal,elevating corticosterone and delaying sleep onset. by contrast,green light (530 nm) produces rapid sleep induction. compared to wildtype mice,these responses are altered in melanopsin-deficient mice (opn4-/-),resulting in enhanced sleep in response to blue light but delayed sleep induction in response to green or white light. we go on to show that blue light evokes higher fos induction in the scn compared to the sleep-promoting ventrolateral preoptic area (vlpo),whereas green light produced greater responses in the vlpo. collectively,our data demonstrates that nocturnal light exposure can have either an arousal- or sleep-promoting effect,and that these responses are melanopsin-mediated via different neural pathways with different spectral sensitivities. these findings raise important questions relating to how artificial light may alter behaviour in both the work and domestic setting. © 2016 pilorz et al.
آدرس sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, department of experimental psychology,university of oxford,oxford, United Kingdom, henry wellcome laboratories for integrative neuroscience and endocrinology,university of bristol,bristol, United Kingdom, department of physiology,anatomy and genetics,university of oxford,oxford, United Kingdom, mrc harwell,harwell science and innovation campus,oxfordshire, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom, sleep and circadian neuroscience institute (scni),nuffield department of clinical neurosciences,oxford molecular pathology institute,dunn school of pathology,university of oxford,oxford, United Kingdom
 
     
   
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