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P. J. Sharp, R. T. Talbot, G. M. Main, I. C. Dunn, H. M. Fraser and N. S. Huskisson

ABSTRACT

The physiological roles of chicken LHRH-I and -II (cLHRH-I and -II) in the regulation of gonadotrophin release were investigated in the domestic chicken. Measurements of the neuropeptides, using specific radioimmunoassays, in brain sections cut in three planes or in grossly dissected brain areas, showed that cLHRH-II occurs in low amounts throughout the brain whereas cLHRH-I is most abundant in the diencephalon. Within the diencephalon, the largest amount of cLHRH-I occurred in the median eminence of the hypothalamus. The amount of cLHRH-I in the median eminence was higher (P<0·05) in laying than in out-of-lay hens. No cLHRH-II was detected in the median eminence in either reproductive state. The amount of cLHRH-I in the hypothalamus was increased (P<0·05) in cockerels at the onset of puberty and in somatically immature birds after castration. There were no correlated changes in the amounts of hypothalamic cLHRH-II measured in the same experimental samples.

Active immunization of laying hens against cLHRH-I but not against cLHRH-II resulted in the complete regression of the reproductive system and a depression in the concentration of plasma LH.

These observations, taken together, suggest that gonadotrophin secretion in the hen is more likely to be directly regulated by cLHRH-I than by cLHRH-II.

Journal of Endocrinology (1990) 124, 291–299

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P A Fowler, M Fraser, P Cunningham, P G Knight, B Byrne, E A McLaughlin, P G Wardle, M G R Hull and A Templeton

Abstract

Ovine and rat pituitary bioassays for gonadotrophin surgeattenuating factor (GnSAF) were utilized to determine whether the level of GnSAF bioactivity in pooled human follicular fluid (hFF) from superovulated women varied according to follicle diameter (≤11 mm, 12–15 mm and 16–21 mm follicles examined using the ovine bioassay, or ≤10 mm, 11–13 mm, 14–17 mm, 18–20 mm, 21–24 mm and ≥ 25 mm follicles examined using the rat bioassay). When tested using dispersed ovine pituitary cells, GnSAF bioactivity, expressed in terms of the reduction in gonadotrophin-releasing hormone (GnRH)-induced LH secretion, was inversely related to follicle diameter (P<0·01). In response to 5 μl hFF/well from follicles of ≤ 11, 12–15 and 16–21 mm diameter, GnRH-induced LH secretion was reduced to 40·5±6·6.9%, 65·2±6·6% and 83·7±7·9% of control respectively. A similar inverse relationship was observed when a second batch of hFF samples from different sized follicles was tested using rat pituitary cell monolayers. Expressing GnSAF bioactivity in terms of the dose required to suppress GnRH-induced LH secretion by rat pituitary cells to 50% of the maximal suppression observed (ED50), the three smallest follicle size pools contained the most GnSAF (ED50 values of 0·13, 2·79 and 5·36 μl hFF/well from follicles of ≤ 10, 11–13 and 14–17 mm respectively). The ED50 values for follicles of 18–20, 21–24 and ≥25 mm were 8·81, 27·1 and 60·0 μl hFF/well respectively. Thus hFF from follicles ≤ 11 mm was over 450 times more potent than hFF from follicles ≥ 25 mm in suppressing GnRH-induced LH release. The ED50 values for inhibin bioactivity (measured as the suppression of basal FSH secretion from rat pituitary monolayers) were much less variable than those for GnSAF bioactivity (between 0·85 and 0·13 μl hFF/well). Inhibin immunoreactivity, measured by a two-site immunoradiometric assay, followed the same pattern as inhibin bioactivity with lowest concentrations in the smallest follicles (41·96 ng/ml) and highest concentrations in the three largest follicle size groups (56·48–64·48 ng/ml). The specific effects of inhibin on GnRH-induced LH and basal FSH release in these pituitary bioassays were determined by incubating culture dishes with pure recombinant human inhibin at doses of 0·025–25 ng/well. In both the sheep and rat pituitary monolayers, basal FSH was suppressed (ED50=0·02 and 0·16 ng/well respectively). However, while inhibin markedly stimulated GnRH-induced LH secretion from ovine pituitary monolayers (ED50=0·04 ng/well), it suppressed GnRH-induced LH secretion from rat pituitary monolayers (ED50=0·31 ng/well) by 13%. The divergent effects of inhibin on GnRH-induced LH secretion in the two culture systems, and the relative insensitivity of GnRH-induced LH secretion to recombinant human inhibin in the rat system, indicates that the inverse relationship between GnSAF concentrations and follicular diameter cannot be an artefact of inhibin bioactivity. In addition, when hFF was fractionated by hydrophobic interaction chromatography using phenyl Sepharose, fractions which contained the greatest amounts of GnSAF bioactivity differed from those which contained peak levels of bioactive or immunoreactive inhibin. These results support in vivo observations that small follicles are important regulators of gonadotrophin secretion in superovulated women. Concentrations of GnSAF fall as the follicles approach an ovulatory size which enables positive steroid feedback on pituitary responses to hypothalamic GnRH, leading to the preovulatory LH surge.

Journal of Endocrinology (1994) 143, 33–44

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Ping Ye, Christopher J Kenyon, Scott M MacKenzie, Katherine Nichol, Jonathan R Seckl, Robert Fraser, John M C Connell and Eleanor Davies

Using a highly sensitive quantitative RT-PCR method for the measurement of CYP11B1 (11β-hydroxylase) and CYP11B2 (aldosterone synthase) mRNAs, we previously demonstrated that CYP11B2 expression in the central nervous system (CNS) is subject to regulation by dietary sodium. We have now quantified the expression of these genes in the CNS of male Wistar Kyoto (WKY) rats in response to systemic ACTH infusion, dexamethasone infusion, and to adrenalectomy. CYP11B1 and CYP11B2 mRNA levels were measured in total RNA isolated from the adrenal gland and discrete brain regions using real-time quantitative RT-PCR. ACTH infusion (40 ng/day for 7 days, N=8) significantly increased CYP11B1 mRNA in the adrenal gland, hypothalamus, and cerebral cortex compared with animals infused with vehicle only. ACTH infusion decreased adrenal CYP11B2 expression but increased expression in all of the CNS regions except the cortex. Dexamethasone (10 μg/day for 7 days, N=8) reduced adrenal CYP11B1 mRNA compared with control animals but had no significant effect on either gene's expression in the CNS. Adrenalectomy (N=6 per group) significantly increased CYP11B1 expression in the hippocampus and hypothalamus and raised CYP11B2 expression in the cerebellum relative to sham-operated animals. This study confirms the transcription of CYP11B1 and CYP11B2 throughout the CNS and demonstrates that gene transcription is subject to differential regulation by ACTH and circulating corticosteroid levels.

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D. St.J. O'Reilly, W. D. Fraser, M. D. Penney, F. C. Logue, R. A. Cowan, B. C. Williams and G. Walters

ABSTRACT

Six male volunteers were infused with arginine (0·5 g/kg body weight) over 30 min, after an overnight fast and water deprivation. There was a significant decrease in renal phosphate clearance (P<0·025) and urinary cyclic adenosine monophosphate (cAMP) output (P<0·025) during the 60- to 90-min period after the beginning of the infusion; both returned to the preinfusion basal levels within 150 min. The plasma levels of parathyroid hormone (PTH) were not affected by the infusion and remained unchanged during the subsequent 150 min. Plasma levels of arginine vasopressin (AVP) were also not significantly affected although plasma osmolality increased by 6–9 mmol/kg in all subjects. The infusion resulted in a diuresis, and a fall in urine osmolality but a decrease in free-water clearance; creatinine clearance was not affected. Six other subjects were given a bolus of 230 i.u. PTH intravenously, and 20 days later this was repeated during an infusion of arginine (0·5 g/kg body weight). There was a significant decrease in urinary phosphate (P< 0·025) and cAMP excretion (P<0·05) when PTH was given with arginine. It is suggested that arginine blocks the action of PTH on the proximal renal tubule but not that of vasopressin on the distal nephron and collecting ducts.

J. Endocr. (1986) 111, 501–506