Serum prolactin response to thyrotropin releasing hormone in estrogen treated hypophysial stalk-transected gilts

Twelve crossbred gilts, 169 ± 3 days of age and 72.8 ± 3.4 kg body weight, were hypophysial stalk-transected (HST)1 or sham hypophysial stalk-transected (S-HST). Gilts were ovariectomized 6 days later and assigned to four treatments of 3 gilts each in a 2 × 2 factorial arrangement. One-half of the HST and S-HST gilts received 5 mg estradiolbenzoate (EB) or corn oil vehicle im at 0800 hr daily for 5 days beginning 64 ± 3 days after HST or S-HST. Blood was collected by jugular vein cannula at 0830 and 0900 hr the day after the last injection of EB or oil. Immediately after the 0900 hr sample, 200 μg thyrotropin releasing hormone (TRH) were injected (iv). Mean basal serum prolactin (PRL) concentration was similar for HST (10.3 ± 1.0 ng/ml) and S-HST (12.3 ± 1.7 ng/ml) gilts, however mean basal serum PRL concentration was greater (P<.05) for EB-treated gilts (13.7 ± 1.3 ng/ml) than for oil-treated gilts (8.8 ± .5 ng/ml). Mean serum PRL concentration of all gilts increased within 10 min and returned to approximately 20 ng/ml by 150 min after TRH. Maximum serum PRL concentrations at 10 min after TRH were greater (P<.01) for S-HST (255.9 ± 29.6 ng/ml) than HST gilts (83.4 ± 18.8 ng/ml), but were not different for EB (198.0 ± 50.6 ng/ml) and oil-treated gilts (141.4 ± 36.3 ng/ml). Area under the serum PRL response curve after TRH was greater (P<.005) for S-HST than HST gilts and for EB than oil-treated gilts (P<.05). These results do not eliminate the possible influence of estrogen on PRL secretion at the hypothalamus, but do indicate that estrogen directly stimulated the anterior pituitary gland to secrete PRL.