Figure 5.

Exposure to light at CT15 induced PER1-ir in SCN above cage movement control levels with a latency of many hours, and this effect differed with genotype. (A) The number of PER1-ir cells increased in the ventral mid-SCN of duper hamsters exceeded that of cage movement controls 9h after the light pulse (p=0.004). In WT hamsters, the light pulse increased the number of PER1-ir cells at latencies of both 6h (p=0.008) and 9h (p=0.006). (B) The number of PER1-ir cells increased in the dorsal mid-SCN of duper hamsters exposed to light at CT15 exceeded that of cage movement controls both 6h (p=0.0001) and 9h (p=0.04) after treatment, but no such effect was evident in WT hamsters. (C) At both 6h and 9h after the light pulse, the number of PER1-ir cells was increased in the ventral portion of the caudal SCN of both duper (p=0.004 and p=0.0003) and WT (p=0.0004 and p=0.004) hamsters. (D) The number of PER1-ir cells was increased in the dorsal portion of the caudal SCN of duper hamsters 6h and 9h after light exposure at CT15 (p=0.002 and p=0.04), but no statistically significant effect was evident in WT hamsters. (E, F) 3h after treatment, the intensity of PER1-ir staining was greater in light-exposed than control WT hamsters in both ventral (p=0.04, E) and dorsal (p=0.03, F) SCN, but the light pulse had no significant effect at any latency in duper hamsters. At CT15, PER1-ir intensity of free running WT hamsters exceeded that of duper mutants in dorsal SCN (p=0.02).