No abstract

Short photoperiods decrease gonadotropin secretion in Siberian hamsters, but it is unknown whether the negative feedback effects of androgens are amplified under such conditions, as is the case in other species. Photoperiod regulates the synthesis and secretion of gonadotropin-releasing hormone (GnRH), beta-endorphin, and arginine vasopressin (AVP), which influence gonadotropin release and sexual behavior but are themselves regulated by gonadal steroid hormones. To determine the role of androgen in these effects of daylength, immunostaining and gonadotropin concentrations were examined after 8 wk of exposure to long or short days (LD or SD). Animals were either left intact, castrated, or castrated with immediate or delayed replacement of testosterone (T). We also investigated effects of age on photoperiodic influences on brain peptides and serum hormone levels. Serum prolactin concentrations were regulated by photoperiod and by gonadal status in LD hamsters. Effects of T on follicle-stimulating hormone secretion were more pronounced in SD hamsters. Older hamsters were generally less responsive to effects of daylength on pituitary function. Photoperiod and gonadal status regulated the number of AVP-immunoreactive (ir) cells in the bed nucleus of the stria terminalis and the medial amygdala. Androgen treatment yielded more AVP-ir neurons in LD than in SD. Photoperiod influenced the number of GnRH-ir cells only in the medial septum of castrated hamsters. Daylength regulated beta-endorphin-ir neurons in intact hamsters, but not in castrates. Only among old hamsters did photoperiod affect the influence of T on beta-endorphin staining in neurons and fibers. Such fiber staining was unaffected by photoperiod in intact and T-treated castrate hamsters, but was reduced in SD castrates. We conclude that daylength modulates the effects of androgen on gonadotropin secretion and influences the effect of T on neuropeptide staining in regionally specific patterns that depend on the age of the animal and its history of prior steroid exposure.