Search Results

You are looking at 1 - 2 of 2 items for

  • Author: P. Shrenker x
Clear All Modify Search
Restricted access

P. Shrenker and A. Bartke


In the male rat, hyperprolactinaemia is associated with significant reductions in plasma LH and FSH levels and in several measures of copulatory behaviour. In contrast to this situation, experimental induction of hyperprolactinaemia in male mice and hamsters is associated with an increase in plasma gonadotrophin levels. It was therefore of interest to determine the effects of hyperprolactinaemia on the copulatory behaviour of these animals. Hyperprolactinaemia was induced by transplantation of pituitaries from adult females and sexual behaviour was tested in the presence of ovariectomized, oestrogen- and progesterone-treated females. Because hyperprolactinaemia increases plasma testosterone levels in intact male hamsters, the animals were castrated and implanted with testosterone-filled silicone elastomer capsules before induction of hyperprolactinaemia. In mice of two inbred strains, DBA/2J and C57BL/6Bg, hyperprolactinaemia appeared to stimulate male sexual behaviour as shown by a significant increase in the proportion of animals mating (C57BL/6) and a significant decrease in mount (DBA/2J) and intromission (C57BL/6Bg and DBA/2J) latencies. Similarly, hyperprolactinaemia did not suppress male copulatory behaviour in the hamster. In contrast, in two experiments in which the animals were tested three times for sexual behaviour, mount or intromission latencies were significantly reduced in pituitary-grafted, as compared with sham-operated males, in the first of the tests. Thus, in the mouse and the golden hamster, experimentally induced chronic hyperprolactinaemia stimulates both gonadotrophin release and male copulatory behaviour. These observations, together with the association of suppressive effects of hyperprolactinaemia on plasma LH and FSH levels and on sexual behaviour in the male rat, suggest the possible existence of a common mechanism underlying both endocrine and behavioural effects of hyperprolactinaemia. We suggest that the suspected effects of hyperprolactinaemia on the release of endogenous LHRH in the hypothalamus may represent such a mechanism.

J. Endocr. (1987) 112, 221–228

Restricted access

P. Shrenker, R. Stegar and A. Bartke


From day 1 post partum to postnatal day 5, lactating female mice were given daily oral doses of 25 μl sesame oil, 0·5 mg tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo(b,d)pyran-1-ol (Δ9-tetrahydrocannabinol; THC)/kg or 50 mg THC/kg in 25 μl oil. Additionally, the pups were given 20 μl oil, 10 μg testosterone or 20 μg testosterone in 20 μl oil s.c. from days 1 to 5 of age. This regimen resulted in nine treatment groups. At 60 days of age, all males were castrated and their testes weighed. After castration, each mouse was implanted s.c. with a 5 mm length of testosterone-filled silicone elastomer capsule. When adult they were tested for male copulatory behaviour. Following behavioural testing the animals were bled by cardiac puncture for measurement of plasma testosterone levels, and their hypothalami removed and assayed for dopamine, noradrenaline, 5-hydroxytryptamine (5-HT) and LH-releasing hormone (LHRH). In addition, another two groups of pregnant females were given daily oral doses of 0·5 or 50 mg THC/kg or oil during the first 3 or 5 days of lactation. The male pups were either decapitated for collection of trunk blood or homogenized for determination of serum or whole body testosterone concentrations. Neonatal administration of THC altered adult male sexual responses and had no effect on hypothalamic noradrenaline, 5-HT and LHRH concentrations. There were large increases in serum testosterone concentrations in neonates after maternal THC treatment, although these differences were not significant. Additionally, THC did not influence the testosterone content of neonatal tissue or the testosterone concentration of adult plasma.

These results suggest strongly that the effect of THC on male sexual responses is not mediated by its effect on adult hypothalamic neurotransmitter concentrations. Some other potential mechanisms are discussed.

J. Endocr. (1986) 110, 517–523