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A. BARTKE, K. S. MATT, T. M. SILER-KHODR, M. J. SOARES, F. TALAMANTES, B. D. GOLDMAN, M. P. HOGAN, A. HEBERT, Does Prolactin Modify Testosterone Feedback in the Hamster? Pituitary Grafts Alter the Ability of Testosterone to Suppress Luteinizing Hormone and Follicle-Stimulating Hormone Release in Castrated Male Hamsters, Endocrinology, Volume 115, Issue 4, 1 October 1984, Pages 1506–1510, https://doi.org/10.1210/endo-115-4-1506
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Adult male golden hamsters maintained in a long photoperiod (14 h of light and 10 h of darkness) or in a short photoperiod (5 h of light and 19 h of darkness for 7 weeks) were castrated and either given one anterior pituitary transplant under the kidney capsule or sham-operated. Additional animals were castrated and grafted or sham-grafted at the time of transfer to the short photoperiod. Starting 2 weeks after castration, all animals were injected three times a week with 20 μg testosterone propionate (TP). After 3 weeks, the dose of TP was increased to 80 jig and, after an additional 2 weeks, to 320 μg per injection. Blood samples were collected 2 weeks after castration and 1 day after the last injection of 20, 80, and 320 μg TP. Short photoperiod reduced and pituitary grafts increased plasma PRL levels. Plasma testosterone levels were related to the dose of injected TP, but were not influenced by photoperiod or pituitary transplants. Before the onset of TP injections, plasma LH and FSH levels in grafted and sham-grafted hamsters did not differ. In each of the three photoperiod conditions, injections of TP were consistently less effective in suppressing plasma gonadotropin levels in pituitary-grafted animals than in shamgrafted controls. These results indicate that 1) PRL modulates the effects of exogenous testosterone on LH and FSH release in adult castrated male golden hamsters, 2) this effect of PRL is due to reducing the sensitivity of the hypothalamic-pituitary system to feedback inhibition by testosterone, and 3) suppression of pituitary PRL release in short photoperiod may be partially responsible for the concomitant increase in the sensitivity of LH and FSH release to inhibition by testosterone. (Endocrinobgy115: 1506–1510, 1984)
