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Alan C. Rupp, Cara M. Altimus, Samer Hattar; Melanopsin Drives Acute Light-Dependent Changes in Body Temperature Against Cone-Mediated Inhibition. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3463.
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It's currently unclear how the three retinal photoreceptors--rods, cones, and ipRGCs--individually contribute to light-dependent changes in body temperature. Previous work has shown that acute light treatment at night results in reductions in wheel-running activity and the induction of sleep. Interestingly, wheel-running inhibition is dependent on rods/cones and melanopsin phototransduction pathways, whereas sleep is predominantly regulated by the melanopsin pathway. Since we observed differences in acute light effects on wheel-running versus sleep, we sought to use acute light effects on body temperature to address the contribution of the rods, cones, and ipRGCs to a distinct non-image forming visual function.
Mice were maintained on a 12:12 light-dark cycle and were administered a 3-hour light pulse at ZT14 (2 hours after lights are turned off). Core body temperature was measured using telemetric probes implanted in the abdominal cavity and data was collected in 2-minute intervals.
Body temperature at night is ~2 °C higher than during the day. In response to a 3-hr light pulse at night, wild-type mice show a rapid 1 °C reduction in body temperature compared to the previous night. This reduction is completely lost in melanopsin knock-out mice. In contrast, two separate mouse lines in which ipRGCs are the only functional photoreceptors (MO) show two distinct outcomes: One line shows similar reduction in body temperature to WT animals, whereas the other line shows delayed and transient responses. The only difference between these two is the state of the cones, with the WT-like MO responder having cones in the dark state and the weak responder cones in the light. In agreement with the inhibitory effect of cones on temperature changes, animals that have rod phototransduction knocked out show attenuated responses to the light pulses.
Our results indicate that melanopsin and rods are responsible for generating the full effect of the acute reduction in body temperature to a light pulse at night. Surprisingly, in the absence of rod input, activation of cones either by light or through mutations leads to the attenuation of light effects on temperature. These studies indicate that the effects of light on sleep should be re-evaluated in light of these new discoveries.
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