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. 2006 Dec 13;26(50):12984–12995. doi: 10.1523/JNEUROSCI.4253-06.2006

Figure 3.

Figure 3.

Disruption of Dexras1 potentiates the effects of late-night light exposure. A, B, Representative actograms of wheel-running activity of dexras1+/+ (A) and dexras1−/− (B) mice. Mice were exposed to a single 40 lux light pulse for 15 min at ZT 20 (red asterisk), exactly as described in Figure 1. Activity onsets are indicated by blue lines. C–E, Immunohistochemical analysis of p-ERK (C), c-Fos (D), and Per2 (E) expression in response to a single 15 min light pulse at CT 20. Wild-type (+/+) and knock-out (−/−) mice were killed 0.5, 2, and 6 h after the light treatment, and brain sections were processed for phospho-ERK, c-Fos, and Per2, respectively. Dark control animals were not exposed to light but were killed at the same circadian time. F, Quantitation of p-ERK expression in the SCN. Data are presented as mean ± SEM densitometric intensity. Light-induced ERK activation was significantly enhanced in the SCN of dexras1−/− mice relative to wild-type controls. n = 4–6 animals per group. *p < 0.05, ***p < 0.001 (two-tailed Student's t test). G, Quantitation of c-Fos expression in the SCN. Data are presented as mean ± SEM c-Fos-immunoreactive nuclei per SCN section. There was a significantly greater number of c-Fos-immunoreactive nuclei in the SCN of dexras1−/− versus wild-type mice under basal conditions at CT 22 and 2 h after light treatment at CT 20. n = 6–7 per group. **p < 0.01, ***p < 0.001 (two-tailed Student's t test).