Brief light stimulation during the mouse nocturnal activity phase simultaneously induces a decline in core temperature and locomotor activity followed by EEG-determined sleep

Abstract

Light exerts a variety of effects on mammals. Unexpectedly, one of these effects is the cessation of nocturnal locomotion and the induction of behavioral sleep (photosomnolence). Here, we extend the initial observations in several ways, including the fundamental demonstration that core body temperature (T(c)) drops substantially (about 1.5°C) in response to the light stimulation at CT15 or CT18 in a manner suggesting that the change is a direct response to light rather than simply a result of the locomotor suppression. The results show that 1) the decline of locomotion and T(c) begin soon after nocturnal light stimulation; 2) the variability in the magnitude and onset of light-induced locomotor suppression is very large, whereas the variability in T(c) is very small; 3) T(c) recovers from the light-induced decline in advance of the recovery of locomotion; 4) under entrained and freerunning conditions, the daily late afternoon T(c) increase occurs in advance of the corresponding increase in wheel running; and 5) toward the end of the subjective night, the nocturnally elevated T(c) persists longer than does locomotor activity. Finally, EEG measurements confirm light-induced sleep and, when T(c) or locomotion was measured, show their temporal association with sleep onset. Both EEG- and immobility-based sleep detection methods confirm rapid induction of light-induced sleep. The similarities between light-induced loss of locomotion and drop in T(c) suggest a common cause for parallel responses. The photosomnolence response may be contingent upon both the absence of locomotion and a simultaneous low T(c).

Melanin-concentrating hormone neurons specifically promote rapid eye movement sleep in mice

“…In addition, if there was leakage of light from the fiber optic cable or its connectors, the increase in NREM sleep and EEG delta power following the photostimulation of MCH neurons (Konadhode et al, 2013) could have resulted from direct effects of light pulses applied during the dark (photostimulation in sham-injection controls were not studied). Even millisecond light pulses during the dark period in nocturnal animals can increase NREM sleep and EEG delta power for long durations even after withdrawal of light (Morin and Studholme, 2009, Studholme et al, 2013). Finally, light penetration may be insufficient to activate all transfected MCH neurons, as they are spread over a large area (~ 1.5 mm mediolatareally, ~1 mm rostrocaudally; ~1.2 mm dorsoventrally).…”

Drugs that prevent mouse sleep also block light-induced locomotor suppression, circadian rhythm phase shifts and the drop in core temperature

“…In addition to its locomotion suppression effects, light also induces a large decline in core body temperature (Tc; (Studholme et al, 2013)). Tc is normally lowest during the daylight hours when most nocturnal species sleep and, regardless of time of day, is lower during sleep than during wake (Obal et al, 1985).…”

“…We have suggested elsewhere that light-induced circadian rhythm phase shifts, locomotor suppression/photosomnolence and reduction of body temperature may be controlled via a common retinal input pathway (Morin, 2013b, Studholme et al, 2013). The present studies were designed to determine whether the three psychostimulant drugs are able to prevent these responses with the expectation that if a drug blocked one of the responses to light, it would block them all.…”

Acute effects of light on the brain and behavior of diurnal Arvicanthis niloticus and nocturnal Mus musculus

“…These areas might produce acute effects on general activity via pathways extending to structures that regulate sleep/wake state [5], as light can rapidly trigger sleep in nocturnal mammals (e.g. mice [61–62]) and heighten arousal/alertness in diurnal ones (e.g. humans [63]).…”