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C L Sisk

Publications and source records attributed to C L Sisk.

40 records · Page 3Linked to original sources

Reproductive responsiveness to short photoperiod develops postnatally in male golden hamsters.

The development of the reproductive response to short photoperiod in golden hamsters was examined by monitoring testis size in hamsters that were either: raised on 14L:10D from birth; raised on 6L:18D from birth; or born on 14L:10D and transferred to 6L:18D at either 1, 2, 3, 4, 5, 6, 7, 9, or 12 weeks of age. Testis growth occurred between 3 and 7 weeks of age at similar rates in all groups. Testicular regression occurred in all groups exposed to short days; the time of regression depended on the age of the animals when they were first transferred to 6L:18D. Testicular regression began at about 10 weeks of age in all groups transferred to 6L:18D between birth and 5 weeks of age. In contrast, regression began at 11.2, 13.3, 15.6, and 18.2 weeks of age in hamsters transferred to 6L:18D at 6, 7, 9, and 12 weeks of age, respectively. These results suggest that the reproductive system of male hamsters is refractory to the inhibitory effects of short days on reproductive function until 5 to 6 weeks of age. Thereafter, exposure to short days initiates testicular regression in hamsters within 5 to 7 weeks.

Aging↗

LHRH in the ferret: pubertal decrease in the number of immunopositive arcuate neurons.

This study correlated a region-specific change in the number of luteinizing hormone-releasing hormone-immunopositive (LHRH+) neurons with pubertal development in male ferrets. There were 50% fewer LHRH+ cell bodies in the arcuate nucleus of peri- and postpubertal ferrets than in prepubertal ferrets; this significant decrease represented a 15% reduction in the overall number of LHRH+ neurons. Intracerebroventricular colchicine did not reveal additional numbers of LHRH+ neurons in the arcuate nucleus, indicating that the pubertal decrease in arcuate LHRH+ cell bodies was not due to rapid transport of peptide. These results suggest that LHRH of arcuate origin may inhibit release of LHRH via ultrashortloop negative feedback in prepubertal ferrets. Cessation of peptide production in half of the arcuate LHRH neurons at puberty could result in a reduction in this inhibitory signal that permits the pubertal increase in LHRH/LH release. Alternatively, LHRH of arcuate origin may have a nonpituitary role. In either case, these data provide evidence for heterogeneity of function among LHRH+ neurons.

Animals↗