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Search for other papers by K. M. Kendrick in
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Search for other papers by A. F. Dixson in
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ABSTRACT
Hyperprolactinaemia was induced in castrated, testosterone-treated male rats using ectopic pituitary grafts under the kidney capsules. After 6 weeks the absolute refractory period of stria terminalis neurones in these animals did not differ significantly from long-term castrated rats (mean = 1·72 vs 1·69 ms) in spite of the presence of normal testosterone concentrations. Gonadally intact animals, and sham-operated castrated animals treated with testosterone, showed by comparison the characteristic significantly shorter absolute refractory period normally associated with testosterone stimulation (mean = 1·15 and 1·08 respectively). These results provide the first demonstration that hyperprolactinaemia can abolish central sensitivity to testosterone.
J. Endocr. (1984) 102, 109–113
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ABSTRACT
Unlike in other non-human primates, ovariectomy of the female marmoset did not alter heterosexual interactions. Proceptive behaviour bouts retained the same cyclicity, duration and frequency within tests as during the ovarian cycle. Significant rises in plasma levels of cortisol, progesterone, oestrone and testosterone were found during these proceptive behaviour bouts and in cortisol, progesterone and oestrone at their onset. Results suggest a role for adrenocortical steroids in both maintaining female sexuality and regulating its cyclicity during ovarian cycles in this primate.
J. Endocr. (1984) 101, 155–162
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ABSTRACT
Stressful stimuli associated with aggressive encounters and low social rank may affect female fertility in a variety of mammalian species. In these experiments we examined the effects of aggressive encounters and physical restraint in a primate chair on the patterns of LH secretion in ovariectomized, oestrogen-primed female marmosets. Receipt of aggression from a female conspecific, followed by physical restraint for collection of blood samples (at 10-min intervals for 4 h), resulted in marked declines in LH concentrations during oestradiol-induced LH surges in five animals (from 112 ± 24 μg/l to 45±12 μg/l; group means ± s.e.m.; P<0·05). This was due to reductions in LH pulse amplitude rather than to changes in pulse frequency. Decreases in plasma concentrations of LH were reversed by treating females with exogenous LH-releasing hormone (LHRH). Cortisol treatment had no effect on LH levels during oestrogen-induced LH surges. Effects of aggressive encounters and physical restraint on plasma LH were not therefore due to reduced pituitary responsiveness to LHRH or to increased plasma concentrations of cortisol. In separate experiments it was found that physical restraint alone had no effect on plasma LH in habituated subjects, and that decreases in plasma LH after receipt of aggression only occurred if animals were subsequently placed in the restraint chair. A summation of stressful effects is therefore required to produce the fall in circulating LH. A summation of social and other environmental stressors may also underlie the reduced fertility seen in free-living animals.
J. Endocr. (1988) 118, 259–264
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ABSTRACT
The use of pituitary desensitization by an LHRH agonist (buserelin) to examine pituitary-testicular function was investigated in a New World primate. Six adult male marmoset monkeys were injected s.c. with an LHRH agonist implant (1·5 mg in a rod 0·5 cm long). Pharmacokinetics, determined by radioimmunoassay of urinary buserelin, revealed a rapid initial release of the agonist followed by a steady decline during a 200-day period. The LHRH agonist treatment resulted in a rapid initial rise in plasma LH followed by a return to mean values similar to those seen in the control samples by 7 days after implantation. Using the present protocol, no evidence of subsequent pituitary desensitization or suppression of testicular function was observed, plasma concentrations of LH and testosterone remaining within the normal range during the 200-day study period.
In contrast, pituitary-testicular function was suppressed in the male marmoset after blockade of pituitary LHRH receptors by an LHRH antagonist. Five adults were treated with a single s.c. injection of the antagonist [Ac-d-Nal(2)1,d-pCl-Phe2,d-Trp3,d-Ser(Rha)6,AzGlyNH2 10]-LHRH at a dose of 300 μg/kg. The LHRH antagonist induced a marked suppression of plasma LH and testosterone by 6–8 h, the low levels being maintained for 24–48 h.
These results show that, whereas treatment with an LHRH antagonist can inhibit pituitary-testicular function in the male marmoset, it may be that desensitization cannot be induced by the LHRH agonist used.
Journal of Endocrinology (1990) 125, 233–239
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ABSTRACT
Plasma levels of vasoactive intestinal polypeptide (VIP) in the corpora cavernosa penis and dorsal penile veins greatly exceeded those measured in the limb or caudal veins during anaesthesia in various mammals (Bennett's wallaby, Barbary sheep, cheetah, puma, sooty mangabey, pigtail macaque and chimpanzee). Tactile stimulation of the penis immediately before or during collection of blood samples resulted in an increase. In the wallaby, VIP levels (mean ± s.e.m.) in blood samples collected from the flaccid penis in the absence of tactile stimulation were very low (0·6 ± 0·5 pmol/l). A 36-fold increase in VIP occurred after manual extension of the flaccid penis (24·8 ± 3·2 pmol/l) or during manually stimulated erections (25· 1 ± 1·7 pmol/l). Electrical stimulation of erection produced no significant increase in VIP levels (2·3±0·9 pmol/l) unless accompanied by tactile stimulation (17·5±1·4 pmol/l). These studies provide the first demonstration that sensory feedback from the penis plays an important role in regulating vasoactive intestinal polypeptidergic activity. Since VIP is a potent vasodilator its release due to tactile stimuli during copulation may play a role in the maintenance of penile erection.
J. Endocr. (1984) 100, 249–252
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We have shown previously that pregnant mare serum gonadotrophin (PMSG) induces ovulation only in rats weighing over 60 g on the day of injection. The under-60 g rats do not ovulate although they secrete a preovulatory surge of a pleiomorphic form of LH. Presumably this pleiomorph is inactive.
Comparisons were made of plasma hormone concentrations in rats treated with PMSG that weighed over and under 60 g. The measurements were made on samples taken between 13.00 and 22.00 h on the day of the expected preovulatory LH surge. Prolactin and corticosterone levels were lower in the lighter group compared with the heavier group. A midday pulse of GH detected in the over-60 g animals did not occur in the under-60 g group. Levels of ACTH were slightly higher in the under-60 g rats and together with the low corticosterone concentrations indicate adrenal insensitivity. Oestradiol, progesterone and TSH concentrations were the same in the two groups. Since progesterone secretion is under LH control, the 'inactive' pleiomorphic form of LH must have steroidogenic activity. There was an indication that the under-60 g rats also secreted a pleiomorphic form of FSH.
Reports in the literature indicate that prolactin, corticosterone and GH have a positive modulatory influence on natural puberty. They may also influence precocious puberty induced by PMSG, since in the unresponsive under-60 g rat plasma levels of these three hormones were low. Perhaps the release of one or more of these hormones is dependent upon the physical maturity of the animal as represented by body weight.
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ABSTRACT
In-vitro data from experiments on rats implicate granulosa cells as primary sites of hormone-dependent ovarian inhibin biosynthesis, but no equivalent data exist for primates. We have used the common marmoset (Callithrix jacchus) to investigate inhibin biosynthesis in primate granulosa cells in vitro and to determine its relationship to preovulatory follicular development. To relate the production of immunoactive inhibin to follicular maturity, we studied primary granulosa cell cultures from follicles at progressive stages of preovulatory development. Granulosa cells from 'large' (≥2·0 mm diameter) follicles expressed high rates of inhibin production and steroidogenesis (progesterone), and were positively regulated by human (h)LH in vitro. Less mature granulosa cells from 'medium' (1·1–1·9 mm) and 'small' (≤ 1·0 mm) follicles expressed proportionately lower rates of inhibin production and steroidogenesis, but each parameter was stimulated in a dose- and time-dependent manner by hFSH in vitro. The stimulatory action of hFSH on immunoactive inhibin was augmented by the presence of testosterone or oestradiol; testosterone (but not oestradiol) also augmented the steroidogenic response to hFSH. Marmoset luteal tissue also produced inhibin in vitro and expressed an ∼1·5 kb inhibin α-subunit mRNA, confirming the corpus luteum as a source of ovarian inhibin in primates.
These results provide direct experimental evidence that primate granulosa cells produce inhibin. They suggest that production of inhibin by immature granulosa cells is initially induced by FSH and subject to modulation by follicular steroids. During advanced preovulatory development, granulosa cell inhibin production becomes directly responsive to LH, thereby indicating a role for LH in the control of peri- and postovulatory inhibin secretion by the primate ovary.
Journal of Endocrinology (1989) 123, 65–73
