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Search for other papers by S. E. Inkster in
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Search for other papers by S. A. Whitehead in
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Summary. Injection of 150 μg 6-hydroxydopamine (6-OHDA) into the third ventricle of rats depleted the mean hypothalamic concentration of noradrenaline by 71% whereas the mean dopamine concentration was only reduced by an insignificant 7%. Isolated perfused pituitary glands taken from intact 6-OHDA-treated rats showed a markedly increased LH response to pulses of LHRH although there was no significant difference in the circulating levels of LH. Ovarian cyclicity was disrupted and the hypothalamic content of LHRH was significantly reduced. Hypothalamic synaptosomes prepared from intact 6-OHDA-treated animals consistently released less LHRH than did controls although the difference was not significant. Noradrenaline, dopamine and adrenaline did not significantly affect LHRH release from experimental or control synaptosome preparations. In ovariectomized rats 6-OHDA treatment did not inhibit the positive feedback effects of progesterone administration to oestrogen-primed animals, although the negative feedback effects of the priming oestrogen treatment was augmented. The results indicate that depletion of hypothalamic noradrenaline causes subtle changes in the endogenous release of LHRH and may alter the negative feedback effects of steroids on the hypothalamic—pituitary axis.
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Summary. An increase in LH secretion was induced in ovariectomized oestradiol benzoate-primed rats 5 h after a second injection of oestradiol benzoate. Lesions stereotaxically placed in the cortical and basomedial amygdala of steroid-primed rats abolished this rise. The results provide evidence for a facilitatory action of the amygdala upon LH release and an involvement of this region of the limbic system in oestrogen-feedback mechanisms.
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The effects of stimulating the immune system with lipopolysaccharide (LPS) or suppressing the immune system with cyclosporin (CS) on reproductive functions in the female rat were investigated. Animals were either treated acutely with LPS (2 mg kg−1) or cyclosporin (20 mg kg−1) on dioestrus day 1 and 2 or treated chronically over a period of 6 days (on alternate days with LPS, daily with CS). Chronic LPS treatment induced a state of constant dioestrus and decreased circulating concentrations of progesterone and oestradiol. Chronic CS treatment induced some irregularity in the 4-day vaginal smear pattern in a minority of animals and, while it had no effect on circulating concentrations of progesterone, oestradiol concentrations were suppressed compared with those measured in pro-oestrous animals. LH responses to GnRH were reduced in both perifused pituitary fragments and cultured pituitary cells obtained from animals pretreated with either LPS or CS. In contrast, a low dose of LPS (20 μg kg−1) given over 6 days did not disrupt ovarian cycles and reduced, but did not abolish, the second phase primed LH response. Neither drug had a direct effect on the pituitary LH responses to GnRH, except that pituitary cells exposed to high doses of CS for periods greater than 48 h did show attenuated LH responses to GnRH. This finding was not paralleled with high doses of LPS. The differential count of ovarian follicles from histological studies showed that LPS treatment was associated with significantly fewer large preovulatory follicles, whereas animals treated with CS showed a similar distribution of follicular volumes compared with controls. Results suggest that the hypothalamic–pituitary control of ovarian function is impaired by both LPS and CS treatment, and LPS appears to have an additional effect in suppressing ovarian functions, possibly via an inhibitory action on steroidogenesis.
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Summary. Domperidone at a dose of 4 mg/kg significantly raised circulating prolactin levels in male and female rats although this increase was approximately 4-fold higher in females compared with males. No effect on LH secretion was observed. The LH and prolactin responses to Gn-RH and TRH respectively were investigated with isolated perfused pituitary glands obtained from domperidone-pretreated animals. For females, the basal release of prolactin was raised by domperidone pretreatment and the responsiveness of the pituitary to Gn-RH was markedly attenuated. When domperidone was added to the perfusing media, high concentrations (100 μg/ml) reduced both the basal and TRH-stimulated prolactin secretion from pituitaries of untreated male and female rats although lower doses (1 μg/ml and 10 ng/ml) were ineffective in altering prolactin release. The pituitary LH responses to Gn-RH were similarly reduced by the presence of 100 μg domperidone/ml in the medium.
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Summary. The time-course of the inhibitory effect of hyperprolactinaemia on LH secretion was delineated. Hyperprolactinaemia was induced in ovariectomized rats with injections of domperidone or ovine prolactin and circulating LH levels were measured from 1 h to 9 days after the treatment. Inhibition of LH secretion occurred within 2–4 h after treatment, and was maintained (provided that serum prolactin remained elevated) for a period of 6 days only. Thereafter LH levels increased to become insignificantly different from control levels on Day 9. A reduction in pituitary responsiveness was not associated with the acute or sub-chronic inhibition of LH secretion, although a significant fall in responsiveness was observed simultaneously with the return of serum LH levels to control values. No changes in hypothalamic LH-RH content was found. It is concluded that an impairment of pituitary function is not responsible for the inhibitory action of prolactin on LH secretion.
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Summary. Adult rats were pretreated with a 3-day regimen of human menopausal gonadotrophin (hMG), PMSG, human FSH or hCG and experiments were carried out on the day of pro-oestrus. Treatment with hMG and hFSH induced a significant increase in the number of preovulatory follicles on the day of pro-oestrus and this was correlated with increased circulating concentrations of oestradiol. There was a parallel increase in the self-priming effect of GnRH, as observed from the biphasic LH response to a continuous GnRH challenge. PMSG treatment did not stimulate increased numbers of maturing follicles and was less effective in raising circulating oestrogen concentrations compared with hMG and hFSH. However, pituitary responsiveness was much higher after PMSG treatment and the biphasic response to continuous perfusion with GnRH was absent; LH release was high from the initiation of the stimulus. hCG alone failed to stimulate follicular maturation but enhanced pituitary LH responses. Hemi-pituitary glands perfused in the presence of isolated preovulatory follicles also showed augmented biphasic LH responses to GnRH compared with control hemi-pituitary glands. The apparent dissociation which can occur between follicular maturation, circulating oestrogen concentrations and pituitary responsiveness to GnRH supports the idea of non-steroidal ovarian factors modulating LH release.
Keywords: luteinizing hormone; gonadotrophin releasing hormone; ovaries; follicles; feedback
Basic Medical Sciences, Cellular and Molecular Medicine, Community Health Sciences, Clinical Developmental Sciences, Divisions of
Search for other papers by A I Qureshi in
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Search for other papers by S A Whitehead in
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Basic Medical Sciences, Cellular and Molecular Medicine, Community Health Sciences, Clinical Developmental Sciences, Divisions of
Search for other papers by H D Mason in
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Histological studies have demonstrated that polycystic ovaries (PCO) contain increased numbers of preantral follicles with a specific increase in primary follicles. Polycystic ovary syndrome is associated with hyperandrogenism and pre- and postnatal androgenisation of primates increases the pool of growing follicles producing changes resembling PCO. In vitro studies could test the hypothesis that androgens alter early folliculogenesis, but conventional culture techniques for small follicles are generally unsuitable in non-rodent species. Our objective was to develop and use a method to investigate the effects of testosterone on early folliculogenesis. We adapted an in ovo technique in which lamb cortical ovarian fragments were grafted onto the chorioallantoic membrane of fertilised chick eggs. Optimal experimental conditions for vascularisation and survival of tissue were determined and the model then used to investigate the effects of testosterone on follicle growth. Eggs were inoculated with testosterone at the time of implantation of the ovarian tissue, which was retrieved 5 days later. Tissue was sectioned and follicles staged and counted. There was no wholesale initiation of primordial follicle growth over the 5-day in ovo culture. Importantly, the proportion of primordial, primary and secondary follicles remained similar to those in unimplanted tissue. Testosterone increased the number of primary follicles by 50% compared with controls, an effect that was largely due to a reduction in atresia. In conclusion, incubation of ovarian cortex with testosterone reproduces the changes in early folliculogenesis reported in histological studies of PCO.
