Effects of hyperprolactinaemia and testosterone on the release of LH-releasing hormone and the gonadotrophins in intact and castrated rats

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Abstract
We have investigated the effect of hyperprolactinaemia on the secretion of LH-releasing hormone (LHRH), LH and FSH in male rats of the PVG strain which were left intact, castrated or castrated and then implanted with either a 10 or 30 mm silicone elastomer capsule containing testosterone (T10 and T30 respectively). Hyperprolactinaemia was produced by pituitary grafts under the kidney capsule. Pituitary stalk blood, for LHRH estimation, and peripheral blood, for LH, FSH and prolactin, were collected under alphaxalone anaesthesia. Pituitary stalk blood was collected during three consecutive periods of 30 min each before, during and after the application of an electrical stimulus to the median eminence (ME). Hyperprolactinaemia significantly reduced the plasma concentrations of FSH in intact rats and the post-castration increase in the plasma concentrations of both LH and FSH. Neither hyperprolactinaemia nor castration had any significant effect on the spontaneous output of LHRH, but castration alone or castration plus implantation of a T30 capsule did significantly reduce the increment in LHRH output produced by ME stimulation, an effect not seen in rats bearing pituitary grafts. The T30, but not the T10 capsules suppressed the post-castration increase in the gonadotrophins, and the inhibitory effect of testosterone was not significantly affected by hyperprolactinaemia. An incidental but important finding was that the presence of pituitary grafts under the kidney capsule reduced the anaesthetic dose of alphaxalone by 63%. These results show that (i) in the male rat the inhibitory effect of hyperprolactinaemia on gonadotrophin secretion is not due to a decrease in the spontaneous release of LHRH, (ii) in contrast to the female rat the post-castration increase in gonadotrophin secretion is not accompanied by an increase in the output of LHRH, (iii) the output of LHRH in response to ME stimulation is affected by castration and testosterone but not by hyperprolactinaemia and (iv) the anaesthetic effects of alphaxalone are potentiated by hyperprolactinaemia, and this may explain in part the potentiation of alphaxalone anaesthesia by oestrogen. J. Endocr. (1985) 104, 35–43