Biology of Reproduction, Vol 20, 719-726, Copyright © 1979 by Society for the Study of Reproduction

Photoperiodic Regulation of Ovine Spermatogenesis: Relationship to Serum Hormones

¹ U.S. Meat Animal Research Center, Agricultural Research, Science and Education Administration, U.S. Department of Agriculture, Clay Center, Nebraska 68933

Serum concentrations of reproductive hormones and spermatogenesis were studied in rams exposed to either decreasing (group 1) or increasing (group 2) photoperiods. Six rams were assigned to each group in late February and maintained in individual pens throughout the study. Room temperature was kept at approximately 18°C for both groups of rams. Light schedules were decreased or increased stepwise from a 12 h light:12 h dark photoperiod so that within 8 weeks, rams were exposed to either short days (8 h light:16 h dark photoperiod) or long days (16 h light:8 h dark photoperiod). Scrotal circumference (testis size) decreased (P<0.05)lO% throughout the experiment in long day rams; however, after an initial decrease, scrotal circumference in short day rams increased (P<0.05)15%. When compared to long day rams, short day rams had 45% heavier (P<0.05) testes, 30% larger (P<0.01) seminiferous tubule diameters and produced nearly twice as many sperm. Histological examination of the germinal epithelium revealed that long days exerted deleterious effects at several points in spermatogenesis. The changes in sperm production of photoperiod-treated rams could be the result of changes in several endocrine systems. Short day rams were characterized by low concentrations of serum prolactin and elevated concentrations of serum testosterone, LH and FSH. On the basis of these findings, we suggest that testicular growth in rams exposed to short day lengths is a response to increased gonadotropin activity. The action of these gonadotropins may be direct on the germinal epithelium of the ram testis or may stimulate spermatogenesis indirectly by enhancing testosterone secretion in interstitial cells.

Note:
ACKNOWLEDGMENTS We wish to acknowledge the Endocrine Study Section, National Institutes of Health, Bethesda, MD, for hormone standards (NIH-LH-S18, NIH-FSH-S10 and NIH-P-S8); Dr. D. J. Bolt, USDA-SEA-AR, for prolactin (DJB-7-0330) antisera; Dr. L. M. Sanford, University of Manitoba, Winnipeg, for FSH antiserum (GP-202-B4) and Dr. G. D. Niswender, Colorado State University, Fort Collins, for LH antiserum used in this study. The technical assistance of Ms. Becky Chmelka, Ms. Marilyn Bierman and Mr. Bruce Larsen is sincerely appreciated.

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