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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