Abstract
Reversible loss of fertility which occurs annually in seasonally‐breeding species appears due to changes in the release of pituitary hormones, the levels of gonadal hormone receptors and the sensitivity of the hypothalamic‐pituitary system to inhibition by gonadal steroids. In the golden hamster, exposure to a short photoperiod causes reduction in plasma prolactin (PRL) levels, loss of testicular LH receptors, and gonadal atrophy. Reduction in plasma PRL is probably not secondary to inhibition of testicular steroidogenesis because it cannot be induced by castration or reversed by administration of testosterone. Treatment of gonadally regressed hamsters with PRL increases testicular weight, spermatogenesis, concentration of LH receptors in the testis and plasma testosterone levels. Prolactin‐producing ectopic pituitary homografts prevent loss of LH receptors and delay gonadal regression in animals transferred from a long to a short photoperiod. Treatment of adult male hamsters with PRL can increase plasma FSH levels. It is concluded that changes in PRL release play an important role in mediating the effects of photoperiod on testicular activity in the golden hamster.
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