This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat. In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone. Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation.

These data provide evidence for ovarian hypersecretion of androgens in ovulatory, as well as anovulatory women with PCO, supporting the concept of abnormal regulation of 17-hydroxylase and (17,20-lyase activity in the ovary. The finding of an equal degree of hyperandrogenaemia in ovPCO and anovPCO groups, even though LH levels were much higher in the latter, suggests that hypersecretion of LH is not the primary cause of ovarian hyperandrogenism. Hyperandrogenism in PCOs may therefore represent an intrinsic abnormality of ovarian theca-interstitial cell function.

The possibility that steroids exert their effects on luteinizing hormone (LH) and prolactin release and female sexual behaviour via altering 7-arninobutyric acid (GABA) synthesis within the hypothalamus was investigated. Ovariectomized rats were treated with e$ther oil, 5 pg oestradiol benzoate (OB) or 5 pg OB plus 0.5 mg progesterone (P) 48 h later; autopsy was carried out 54 h after the OB injection. At this time, both steroid treatments stimulated prolactin release and lordotic activity. OB alone exerted a negative feedback effect on LH release while OB plus P stimulated an LH surge.The brains of the rats in these three treatment groups were microdissected and glutamic acid decarboxylase messenger ribonucleic acid (GAD mRNA) was estimated in specific hypothalamic areas obtained from individual brains; these areas included the preoptic area (POA), ventromedial nucleus (VMN), anterior medial portion of the zona incerta (ZI) and the arcuatehedian eminence area (ARC/ME). GAD mRNA concentrations were assessed by the slot-blotting technique and expressed as a ratio of GAD mRNA: b-actin mRNA.Both steroid treatments significantly reduced GAD mRNA in the ARCIME and ZI and OB plus P also reduced the concentration in the POA, while OB alone had no effect in this area. Neither treatment affected GAD mRNA in the VMN. These results indicate that when steroids stimulate LH and prolactin release and female sexual behaviour, they reduce GABA activity probably by reducing GABA synthesis in the POA, ZI and ARCIME. This suggests that GABA normally has an inhibitory influence on these parameters. G4BA synthesis does not however, appear to be involved in the negative feedback effects of steroids on LH release as measured 54 h after OB treatment.;,-,iminobutyric acid (GABA) is widely distributed in the hypothalmius with its highest concentrations in the preoptic area (POA) aiid ventromedial nucleus (VMN) (1 -3). GABA-containing neurons possess steroid receptors (4, 5 ) and it has becn suggested that sri:roids might exert some of their CNS effects via GABAergic s! stems (6-9). These effects include the control of luteinizing hormone (LH) and prolactin release and sexual behaviour. Rep x t s in the literature indicate that GABA can influence sexual bchaviour in females (10, 11) and has a dual effect on the release of I €1 and prolactin (12, 13). The results show that GABA is inhibitory to LH release in the POA and anterior medial portion o!' the zona incerta (ZI) (14-17). The site of it's stimulatory effect is not really known, although some data indicate that it may be in the medial basdl hypothalamus (12,18,19). Within the hypothalaIlIus GABA stimulates prolactin release, but it is inhibitory at the level of the pituitary (12)(13)(14)20). There are many reports investigating the inter-relationship of the gonadal steroids and GABA, in particular noting the effect of oestrogen and progesterone (P) on GABA activity in specific brain areas. Since GABA is present in both neuronal and glial tissue (1, 21) changes in its concentra...

A PCR was used to detect the genome of Chlamydophila abortus in samples of uterine tissue collected from 304 sheep by a sterile technique at an abattoir. The stage of pregnancy of the sheep was determined by measuring the dimensions of the embryo/fetus, and its morphology was recorded. Only samples from non-pregnant sheep and sheep up to 100 days of gestation were retained; the clinical history of the animals was unknown. The total prevalence of the chlamydial genome was 30.9 per cent, with a significantly higher prevalence in the pregnant animals (46.9 per cent). Higher detection rates were recorded during early gestation than during mid-gestation.