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D. J. A. Eckland, K. Todd and S. L. Lightman

ABSTRACT

Immunoreactive vasopressin and oxytocin were measured in the hypothalamo-hypophysial portal blood of both Long–Evans and homozygous Brattleboro rats. Adrenalectomy caused an increase in vasopressin immunoreactivity in portal blood in the Long–Evans strain, whilst administration of dexamethasone to these adrenalectomized animals resulted in a reduction in portal vasopressin immunoreactivity to levels below those seen in sham-operated animals. This vasopressin immunoreactivity co-eluted with synthetic vasopressin on high-pressure liquid chromatography (HPLC), and diluted in parallel in radioimmunoassay. In Brattleboro rats, however, although vasopressin-like immunoreactivity was detected, the portal concentration did not vary with the adrenal status of the animal, nor did it show the characteristics of standard vasopressin on HPLC or in immunoassay. Oxytocin was present in the portal blood of both Long–Evans and Brattleboro rats at similar very high concentrations, but did not vary in response to adrenalectomy. These results are consistent with a role for vasopressin, but not oxytocin, in the hypothalamic response to adrenalectomy and glucocorticoid feedback. Neither vasopressin immunoreactivity nor oxytocin appear to subserve this role in the homozygous Brattleboro rat.

J. Endocr. (1988) 117, 27–34

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H. MORISHITA, F. NAFTOLIN, R. B. TODD, R. WILEN, I. J. DAVIES and K. J. RYAN

Department of Obstetrics and Gynecology, and Laboratory of Human Reproduction and Reproductive Biology, Harvard Medical School, Boston, Massachusetts 02115, U.S.A.

(Received 19 May 1975)

Testosterone and its ring A reduced metabolite, dihydrotestosterone (DHT), lower gonadotrophin concentrations in weaned rats (Swerdloff, Walsh & Odell, 1972; Naftolin & Feder, 1973). While neonatally administered testosterone causes anovulatory sterility in adult female rats, similar treatment with DHT has no apparent effect upon central neuroendocrine programming (Brown-Grant, Munck, Naftolin & Sherwood, 1971; Whalen & Luttge, 1971), which raises the question of whether DHT can suppress gonadotrophins in the neonatal rat.

In the first experiment, 5-day-old Sprague–Dawley-derived rats (Charles River Farms) were injected s.c. with 100 μg DHT propionate (DHTP), 100 μg testosterone propionate (TP, Eli Lilly & Co.) or the sesame oil diluent, and allowed to develop without further treatment. The injection volume was 25 μl. All animals were weaned on day 20. Daily vaginal

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D. S. Jessop, D. J. A. Eckland, K. Todd and S. L. Lightman

ABSTRACT

We have detected significant amounts of corticotrophin-releasing factor-41 (CRF-41) in the rat hypothalamo-neurointermediate lobe system using a radioimmunoassay and reversed-phase high-performance liquid chromatography. Total amounts of CRF-41 in extracts of median eminence (ME), supraoptic nucleus (SON), paraventricular nucleus (PVN) and neurointermediate lobe (NIL) from control animals were 1076 ± 132, 196 ± 44, 22 ± 7 and 147 ± 50 fmol respectively (means ± s.e.m., n = 6). In animals given 340 mmol NaCl/l instead of tap water to drink for 12 days, no significant changes occurred in the CRF-41 content of the ME, SON or PVN, but CRF-41 content increased more than twofold in the NIL (362 ± 58 fmol). Plasma concentrations of CRF-41 and ACTH in control animals were 23 ± 6 and 51 ± 8 pmol/l respectively. After saline treatment no significant change in plasma CRF-41 was detected (20 ± 8 pmol/l) but concentrations of circulating ACTH were decreased (15 ± 2 pmol/l). The CRF-41 content of both the ME and the NIL was significantly depleted after intracerebroventricular injection of colchicine (414 ± 81 and 34 ± 7 fmol respectively). These data suggest that NIL CRF-41 is of hypothalamic origin and can be regulated by an osmotic stimulus.

Journal of Endocrinology (1989) 120, 119–124

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M. D. Stoneham, B. J. Everitt, S. Hansen, S. L. Lightman and K. Todd

ABSTRACT

In male New Zealand white rabbits, it was shown that oxytocin but not vasopressin concentrations in plasma were markedly raised after ejaculation. In male Wistar rats, oxytocin infused into the internal carotid artery reduced the number of intromissions made before ejaculation but had no other significant effect. Infusion of oxytocin into the third ventricle increased the latencies to the first mount and intromission and lengthened post-ejaculatory refractory periods. It is suggested that oxytocin released into the periphery during coitus, while not essentially involved in ejaculation, may exert effects on the genital periphery. Behavioural effects of centrally administered oxytocin suggest that it may play a role in the neural mechanisms underlying post-ejaculatory refractoriness.

J. Endocr. (1985) 107, 97–106