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We investigated the effects of exposure at ecologically relevant levels of dim light at night (dLAN) on sleep and the 24 h hypothalamic expression pattern of genes involved in the circadian timing ( per2, bmal1 , reverb-β , cry1 , ror-α , clock ) and sleep regulatory pathways (cytokines: tlr4 , tnf - α , il-1β , nos ; Ca 2+ -dependent pathway: camk2 , sik3 , nr3a ; cholinergic receptor, achm3 ) in diurnal female zebra finches. Birds were exposed to 12 h light (150 lux) coupled with 12 h of absolute darkness or of 5 lux dim light for three weeks. dLAN fragmented the nocturnal sleep in reduced bouts, and caused sleep loss as evidenced by reduced plasma oxalate levels. Under dLAN, the 24 h rhythm of per2 , but not bmal1 or reverb-β , showed a reduced amplitude and altered peak expression time; however, clock , ror-α and cry1 expressions showed an abolition of the 24 h rhythm. Decreased tlr4 , il-1β and nos , and the lack of diurnal difference in achm3 messenger RNA levels suggested an attenuated inhibition of the arousal system (hence, awake state promotion) under dLAN. Similarly, changes in camk2 , sik3 and nr3a expressions suggested dLAN-effects on Ca 2+ -dependent sleep-inducing pathways. These results demonstrate dLAN-induced negative effects on sleep and associated hypothalamic molecular pathways, and provide insights into health risks of illuminated night exposures to diurnal animals.

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