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R. J. Lucas, M. A. Cameron, A. R. Barnard, R. A. Hut, X. Bonnefont, G. T. J. van der Horst, M. W. Hankins; Circadian Rhythmicity in the Mouse Electroretinogram and the Effects of Clock-Loss. Invest. Ophthalmol. Vis. Sci. 2008;49(13):180.
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In order to explore the functional endpoints of circadian regulation in the mouse retina we recorded electroretinograms (ERGs) under scotopic and photopic conditions from wild type mice at different points in the circadian cycle, and from transgenic Cry1-/-Cry2-/- mice which lack critical components of the molecular clockwork.
Electroretinograms were recorded from wild type and Cry1-/-Cry2-/- mice under conditions of constant darkness. Cone ERGs were recorded against a rod saturating background (3.7 log W/m2) at two circadian time points (CT6 and CT18). Dark adapted scotopic ERGs (flash intensity -5 to 3 log W/m2) were recorded at four circadian time points CT1, CT6, CT13 and CT 18.
We describe circadian variations in the ERG recorded under coneisolating conditions, comprising a nocturnal decrease in the speed andamplitude of the b-wave (a reflection of second order responses to photoreceptoractivation). By contrast, we did not observe a circadian variation in threshold (rod-mediated) responses of the scotopic ERG. In the case of the Cry1-/-Cry2-/- mice, clock loss had a surprisingly slight effect on retinal function, with both rod and cone ERGs essentially intact in these animals. As predicted, ERGs of Cry1-/-Cry2-/- mice lacked circadian rhythmicity. In fact they had substantially larger and faster cone b-waves than wild types at subjective night indicating a possible default of these animals to a daytime-like physiological state.
Our findings reveal that circadian clocks fine-tune multiple components of mouse retinal circuits according to time of day. Clock loss does not necessarily cause retinal dystrophy and, indeed, some aspects of the retinal light response can be augmented by the abolition of circadian control.
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