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Light exerts a strong non-visual influence on human physiology and behavior. Additionally light is known to affect sleep indirectly through the phase shifting of circadian rhythms, and directly, promoting alertness in humans and sleep in nocturnal species. Little attention has been paid to the direct non-image-forming influence of light until recently with the discovery and emerging knowledge on melanopsin, a photopigment which is maximally sensitive to the blue spectrum of light and expressed in a subset of intrinsically photosensitive retinal ganglion cells. Indeed, the development of transgenic mouse models targeting different phototransduction pathways has allowed researchers to decipher the mechanisms by which mammals adapt sleep to their light environment. This review summarizes the novel concepts and discrepancies from recent publications relating to the non-circadian effects of light on sleep and waking. Specifically, we discuss whether darkness, in addition to light, affects their quality. Furthermore, we seek to understand whether longer sustained periods of light exposure can influence sleep, if the direct photic regulation depends on time of day, and whether this affects the homeostatic sleep process. Moreover, the neural pathways by which light exerts a direct influence on sleep will be discussed including the respective role of rods/cones and melanopsin. Finally, we suggest that light weighs on the components of the flip-flop switch model to induce respectively sleep or waking, in nocturnal and diurnal animals. Taking these data into account we therefore propose a novel model of sleep regulation based on three processes; the direct photic regulation interacting with the circadian and homeostatic drives to determine the timing and quality of sleep and waking. An outlook of promising clinical and non-clinical applications of these findings will be considered as well as directions for future animal and human research.

Study objectives Sleep neurobiology studies use nocturnal species, mainly rats and mice. However, because their daily sleep/wake organization is inverted as compared to humans, a diurnal model for sleep studies is needed. To fill this gap, we phenotyped sleep and waking in Arvicanthis ansorgei, a diurnal rodent widely used for the study of circadian rhythms. Design Video-electroencephalogram (EEG), electromyogram (EMG), and electrooculogram (EOG) recordings. Setting Rodent sleep laboratory. Participants Fourteen male Arvicanthis ansorgei, aged 3 mo. Interventions 12 h light (L):12 h dark (D) baseline condition, 24-h constant darkness, 6-h sleep deprivation. Measurements and results Wake and rapid eye movement (REM) sleep showed similar electrophysiological characteristics as nocturnal rodents. On average, animals spent 12.9 h ± 0.4 awake per 24-h cycle, of which 6.88 h ± 0.3 was during the light period. NREM sleep accounted for 9.63 h ± 0.4, which of 5.13 h ± 0.2 during dark period, and REM sleep for 89.9 min ± 6.7, which of 52.8 min ± 4.4 during dark period. The time-course of sleep and waking across the 12 h light:12 h dark was overall inverted to that observed in rats or mice, though with larger amounts of crepuscular activity at light and dark transitions. A dominant crepuscular regulation of sleep and waking persisted under constant darkness, showing the lack of a strong circadian drive in the absence of clock reinforcement by external cues, such as a running wheel. Conservation of the homeostatic regulation was confirmed with the observation of higher delta power following sustained waking periods and a 6-h sleep deprivation, with subsequent decrease during recovery sleep. Conclusions Arvicanthis ansorgei is a valid diurnal rodent model for studying the regulatory mechanisms of sleep and so represents a valuable tool for further understanding the nocturnality/diurnality switch.

Il s’agit d’un patient de 50 ans hospitalise pour bilan d’une diplopie binoculaire horizontale d’apparition progressive en rapport avec une atteinte clinique du VI droit. Le bilan realise en urgence (IRM, bilan cardiovasculaire) elimine une etiologie neurovasculaire. Le bilan complementaire permet initialement d’eliminer une etiologie metabolique, auto-immune ou neuromusculaire. L’analyse du LCR met en evidence une meningite lymphocitaire. Au plan infectieux, le bilan viral dans le sang et dans le LCR est negatif. La serologie de Lyme dans le sang est negative a 2 reprises. La serologie de la syphilis revient positive dans le sang (VDRL 1/32 ; EIA = 42,1). Le patient est alors initialement traite par penicilline G 4 MUI × 6 par jour dans l’hypothese d’une neurosyphilis. Dans les jours suivants, la serologie de Lyme dans le LCR revient positive en IgG a 12 avec un western blot dirige contre 2 bandes et un index de synthese intra-thecale > 3. Le dosage des IgM anti- Treponema pallidum revient normal (en defaveur d’une infection recente) et la recherche de syphilis dans le LCR est negative. L’IRM de controle avec injection retrouve une prise de contraste diffuse de la dure-mere sus- et sous-tentorielle et une prise de contraste du VI e nerf crânien droit. Le diagnostic de neuro-borreliose de Lyme est donc retenu et le patient est traite par ceftriaxone 2 g/j pendant 21 j. L’evolution clinique retrouve une amelioration partielle de la paralysie oculomotrice. Au total, le diagnostic de neuro-borreliose ne doit pas etre ecarte si la clinique est compatible et meme devant une serologie dans le sang negative. Une co-infection Lyme et syphilis existe et la ponction lombaire ainsi que le suivi serologique permette de differencier une infection recente ou ancienne et une atteinte neurologique ou non. Le traitement de reference de la neurosyphilis reste la penicilline G, mais la ceftriaxone est efficace a la fois sur les spirochetes et rickettsies.