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  • Author: J. M. STEWART x
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M. de la LASTRA, MARIA LUISA FORCELLEDO and J. M. STEWART

Vasopressin increases the ovulatory response to PMSG in immature rats (de la Lastra & Forcelledo, 1970). This effect of vasopressin on ovulation, as well as the similarity between the three terminal amino acids of arginine-vasopressin (AVP) and LH-FSH releasing hormone (LH-FSH-RH), induced us to study the influence of the peptide, Pro-Arg-Gly-NH2 (PAGA), which is the terminal fragment of AVP, on the ovulation induced in adult rats with LH or LH-FSH-RH.

Both LH-FSH-RH and PAGA were synthesized by the solid-phase method, using standard techniques (Stewart & Young, 1969). The normal chloromethylated 1% cross-linked polystyrene was used as support, and α-amino groups were blocked with the tert-butyloxycarbonyl group. Toluenesulphonyl blocking groups were used for histidine- and arginine-side

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G. L. Morgan, R. D. Geisert, J. P. McCann, F. W. Bazer, T. L. Ott, M. A. Mirando and M. Stewart

The progesterone antagonist mifepristone (RU 486) was injected i.m. into ewes during the early luteal phase of the oestrous cycle to test the hypothesis that duration of uterine exposure to progesterone from the corpus luteum initiates luteolysis through the proper timing of endometrial oxytocin receptor expression and pulsatile secretion of PGF coincident with release of luteal oxytocin. In Expt 1, duration of cycle, the PGF metabolite 15-keto-13,14,-dihydro-PGF (PGFM) and oxytocin concentrations were measured in ewes treated on days 5, 6, 7 and 8 of the oestrous cycle with either 2.5 or 5.0 mg RU 486 kg−1 day−1 (n = 4 per group); control ewes (n = 6) were injected i.m. with 80% ethanol (diluent). In Expt 2, the presence of functional uterine oxytocin receptors was determined indirectly on day 12 of the cycle by measuring the plasma PGFM response to oxytocin challenge (20 iu, i.v.) in diluent-treated ewes (n = 3) and in ewes treated with 2.5 mg RU 486 kg−1 day−1 on days 6, 7 and 8 of the oestrous cycle. Duration of the oestrous cycle of control ewes (16 ± 1 days) was extended beyond day 24 (day 0 = oestrus) in 10 of 11 ewes treated with RU 486 as determined by daily exposure of ewes to a ram and by measurement of progesterone concentrations in plasma in the two experiments. Luteolysis (days 14–16) in control ewes was preceded (days 12–15) by pulsatile release of PGFM in plasma and by the presence of functional endometrial oxytocin receptors that responded to oxytocin challenge (day 12) with a significant increase in plasma PGFM concentrations. RU 486 treatment prevented pulsatile PGFM release on days 12–15 and release of PGF following oxytocin challenge on day 12 but not on day 20 when oxytocin administration was repeated. The absence of pulsatile PGFM release in ewes treated with RU 486 on days 12, 13, 14 and 15 in Expt 1 was associated with different plasma oxytocin activity in treated and control ewes in that plasma oxytocin increased from days 12 to 14 in mifepristone-treated but not in control ewes. We conclude that adequate progesterone exposure during the early to mid-luteal phase of the oestrous cycle is essential for initiation of ovarian–uterine mechanisms that lead to luteolysis in ewes.

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H. J. Stewart, D. S. C. Jones, J. C. Pascall, R. M. Popkin and A. P. F. Flint

Page Introduction 2 Structures of genes and mRNA molecules 2 Structure of genes 2 Sequences of promoters and enhancers 3 Signals for terminating RNA synthesis 5 Structure of mRNA molecules 5 Structure of genes coding for reproductive polypeptide hormones and hypothalamic releasing factors 7 Structure of gonadotrophin genes 7 Structure of placental lactogen, prolactin and growth hormone genes 10 Structure of the LHRH gene 12 Inhibin, activin and Müllerian duct-inhibiting hormone 13 Localization of gene products by in-situ hybridization 16 Pre- and post-translational processing 18 Pretranslational processing: differential splicing of RNA 18 Post-translational processing 18 Steroidogenic enzymes and steroid sulphatase 20 Steroid hormone receptors 22 Steroid receptor primary structure: amino acid sequences derived from cloned DNA 23 Steroid hormone receptors and oncogenesis 26 Mechanism of binding of receptors to DNA—the finger hypothesis 27 DNA sequences recognized by steroid receptors in eukaryotic cells 28 Fertilization and early development 30 Expression of

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A. W. LISHMAN, W. J. STIELAU, I. E. DREOSTI, W. A. BOTHA, A. M. STEWART and C. E. SWART

Departments of Animal Science and Biochemistry, University of Natal, Pietermaritzburg, South Africa

The anoestrous condition which follows upon periods of underfeeding in ewes is apparently similar to the normal seasonal anoestrus and is usually manifested as a prolongation (Hunter, 1962) or precipitated onset (Smith, 1962) of the seasonal period of sexual rest. It has been suggested that the ovarian quiescence noted in underfed animals may be the result of pseudohypophysectomy (Mulinos & Pomerantz, 1940; Lamming, 1966; Leathem, 1966).

An acute release of LH at oestrus in ewes has been demonstrated by Niswender, Roche, Foster & Midgley, 1968; Goding, Catt, Brown, Kaltenbach,Cumming & Mole, 1969; Wheatley & Radford, 1969) and it is possible that changes in the pattern of LH release may indicate functional changes in the pituitary of ewes which become anoestrous after periods of inanition. This phenomenon was studied in an attempt to elucidate the mechanism involved in a

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Helen Baines, Margaret O Nwagwu, Edwina C Furneaux, Jane Stewart, Jeffrey B Kerr, Terry M Mayhew and Francis J P Ebling

Testicular development is arrested in the hypogonadal (hpg) mouse due to a congenital deficiency of hypothalamic gonadotropin-releasing hormone synthesis. Previous studies have demonstrated that chronic treatment of these mice with estradiol induces testicular maturation and qualitatively normal spermatogenesis, but it is not known whether these are direct effects via estrogen receptors expressed in the testis, or indirect actions via the pituitary gland. The aim of the current studies was to determine whether the actions of estradiol require the presence of androgens. Sensitive assays revealed that chronic estradiol treatment produced time-dependent increases in pituitary FSH production but no increases in pituitary LH or testicular testosterone content could be detected. As a functional test of androgen dependence, hpg mice were treated for 70 days with estradiol plus Casodex (bicalutamide), an androgen receptor antagonist. Casodex treatment markedly attenuated both the estradiol-induced increase in testicular weight and the proliferation of the seminiferous epithelium, as revealed by morphometric analysis. However, it did not affect the estradiol-induced increase in pituitary FSH content, nor did it affect estradiol-induced increases in the weight of the seminal vesicles and epididymides. We conclude that increased FSH production is not sufficient to explain the increase in testicular development induced by estradiol in hpg mice; there is a requirement for functional androgen receptors for induction of testicular growth.