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In golden hamsters, seasonal changes in day length act via a pineal-dependent mechanism to regulate feedback and behavioral effects of androgen. Endogenous opiates participate in photoperiodically regulated neuroendocrine functions, but the effects of androgen on expression of the gene encoding POMC, the precursor of beta-endorphin, have been controversial. We used quantitative in situ hybridization to examine regulation of POMC messenger RNA (mRNA) by testosterone and to test the hypothesis that short day lengths act through the pineal gland to amplify POMC mRNA expression. We studied intact hamsters and castrates with or without androgen treatment held in long (14 h of light, 10 h of darkness) or short (5 h of light, 19 h of darkness) days for 10 weeks. POMC gene expression differed with rostral-caudal plane, photoperiod, and surgical treatment (castration and testosterone administration). Testosterone increased the number of silver grains in labeled cells throughout the arcuate nucleus, and short day castrates given androgen consistently had more silver grains per labeled cell than did their long day counterparts. Testosterone exerted an inhibitory effect, however, on the number of POMC mRNA-positive cells, and more POMC mRNA-labeled cells were found in the arcuate nucleus of long than short day castrates treated with testosterone. Photoperiod had no significant influence in castrates not receiving androgen. Testosterone treatment had generally similar effects whether it was begun at the time of castration or 5 weeks later. Pinealectomy blocked the influence of photoperiod on both the mean number of silver grains per labeled cell and the number of labeled cells. The results indicate that day length regulates POMC gene expression when androgen levels are held constant, but that androgen is necessary for photoperiod effects to be expressed.

endocrinology

Effects of Photoperiod and Androgen on Proopiomelanocortin Gene Expression in the Arcuate Nucleus of Golden Hamsters**This work was supported by NIH Grants MH-44132 and K02-MH-00914 (to E.L.B.).