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SUMMARY
Electrolytic lesions were made in the hypothalamus of 41 Merino ewes which were subsequently observed for 2–16 months.
Ovarian inactivity resulted from bilateral medial and ventral lesions placed immediately posterior to the optic chiasma (four ewes) or immediately anterior to the mammillary body (five ewes). Failure to show oestrus while apparently still ovulating regularly was a feature in another four ewes in which bilateral medial and ventral lesions were placed between the sites already described. Small bilateral lesions in these ventral regions led initially to ovarian inactivity, but final re-establishment of apparently normal reproductive activity in three ewes. Bilateral lesions in regions other than those described above resulted in no apparent change in reproductive activity (eight ewes). Similarly, unilateral or asymmetrical lesions in the remaining 17 ewes failed to affect their reproductive activity.
The results are consistent with the hypothesis that in sheep a region of the median eminence responsible for the production of gonadotrophin-releasing factors requires neural inputs traversing both anterior and posterior hypothalamic areas.
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Investigation of hypothalamic areas responsible for release of gonadotrophins in sheep required a method for blocking the natural release of ovulating hormone(s). This report describes the results of preliminary observations on the effect of pentobarbitone sodium on ovulation in the ewe.
In Merino ewes the onset of oestrus was determined by testing with vasectomized rams at intervals of no more than 2 hr. When ewes were found to be in oestrus they were either anaesthetized immediately with pentobarbitone sodium given i.v. and kept anaesthetized for 12, 24 or 48 hr., or anaesthetized for 12 or 20 hr. with pento-barbitone sodium commencing 4 hr. after the onset of oestrus or left conscious as controls. Four of the ewes anaesthetized at the beginning of oestrus were injected intramuscularly with 1000 i.u. human chorionic gonadotrophin (HCG) 6 hr. after the onset of oestrus. The ovaries of some ewes were examined at laparotomy 36
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Several authors have reported that, in sheep, electrolytic destruction of certain basal hypothalamic regions leads to ovarian inactivity, or failure to exhibit oestrus, or both (Clegg, Santolucito, Smith & Ganong, 1958; Clegg & Ganong, 1960; Radford, 1967). This paper reports the induction of ovulation in sheep by electrical stimulation of the basal hypothalamus. The experimental approach was based on the fact that when ewes are injected with 750 i.u. pregnant mare serum (PMS) on the last day of a course of progesterone injections (10 mg. i.m./day) and 1000 i.u. human chorionic gonadotrophin (HCG) is injected 24 hr. later, ovulation occurs within the next 30 hr., i.e. 54 hr. after PMS (Braden, Lamond & Radford, 1960; Braden & Moule, 1962). If HCG is not injected, ovulation does not occur until later. On the supposition that electrical stimulation of appropriate hypothalamic regions should substitute for HCG, experiments have been done on ewes
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SUMMARY
The injection of oestradiol benzoate (OB) into the ovariectomized ewe induced a biphasic response in circulating luteinizing hormone (LH). There was a fall in concentration during the first 8–12 h after injection, and then a rapid increase in concentration during the next 12 h. Sodium pentobarbitone anaesthesia, begun either at the time of injection of OB, or 8 or 16 h later, did not affect the first phase, but prevented the second phase of this response. The injection of synthetic luteinizing hormone releasing factor caused a release of LH that was similar both in anaesthetized and conscious ewes. The results indicated a non-nervous site for the inhibitory action of oestrogen on circulating LH, and a central nervous site of action of oestrogen in stimulating LH release.
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An integral part of some current theories on regulation of the oestrous cycle is that increased secretion of oestrogen causes the pre-ovulatory release of luteinizing hormone (LH). The evidence in favour of this concept is, however, equivocal (see McCann, Dhariwal & Porter, 1968), a situation partly attributable to the inadequacy of methods used for the estimation of LH. In the sheep, the pre-ovulatory release of LH occurs during oestrus; this was inferred by Robertson & Hutchinson (1962) on the basis of pituitary content of LH, and was subsequently clearly demonstrated by Pelletier, Kann, Dolais & Rosselin (1968) and Wheatley & Radford (1969) using radioimmunoassay methods to estimate LH in plasma. The sensitivity of these latter methods provided a means of examining the role of ovarian steroids in the oestrous surge of LH in the ewe. This report deals with changes in plasma LH concentration following treatment of ovariectomized ewes with
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Prostaglandin analogues were used to induce luteal regression simultaneously in a number of ewes, thereby synchronizing the final stages of follicular maturation in these animals. Some of the ewes were anaesthetized for 24 h immediately after the injection of prostaglandin (experiment 1), and others for 15 h, starting 24 h after the injection of prostaglandin (experiment 2). In both experiments administration of anaesthetic significantly delayed the onset of oestrus and the time of ovulation relative to prostaglandin-treated control animals. The results from assays of blood samples collected at regular intervals in experiment 1 indicated that the preovulatory peak in the concentration of LH and the periovulatory changes in the concentration of FSH were similarly delayed and that during anaesthesia the level of LH was significantly reduced. It is suggested that the reduced level of LH, which probably resulted from a reduction in the secretion of releasing factor due to anaesthesia, failed to support oestrogen production by the Graafian follicle(s), thereby delaying the occurrence of oestrus and ovulation.
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ABSTRACT
The biological potencies of recombinant human insulin-like growth factor-I (IGF-I) and two of its analogues were examined for hydrogen peroxide release by neutrophils and blastogenesis by mononuclear cells. The binding affinities of these peptides for bovine serum IGF-binding proteins (IGFBPs) and IGF-I receptors on bovine neutrophils and mononuclear cells were also investigated. Relative to control treatment containing no IGF-I, preincubation of neutrophils with 12·5 μg/l of IGF-I, des(1–3)IGF-I (an analogue of human IGF-I lacking the N-terminal tripeptide Gly-Pro-Glu) and long R3 IGF-I (an analogue of human IGF-I with arginine replacing glutamate at position 3 of human IGF-I and the N-terminal extension Met-Phe-Pro-Ala-Met-ProLeu-Ser-Ser-Leu-Phe-Val-Asn) increased the release of H2O2 by 65%, 64% and 32% respectively. However, the difference in stimulating the release of H2O2 between long R3 IGF-I and other two (IGF-I and des(1–3)IGF-I) was reduced at a dosage of 100 μg/l. In the absence or presence of 2·5% fetal calf serum (FCS), 100 μg/l of IGF-I, des(1–3)IGF-I but not long R3 IGF-I significantly stimulated thymidine incorporation into mononuclear cells. In addition, des(1–3)IGF-I was more potent than IGF-I in stimulating thymidine incorporation into mononuclear cells in the presence of 2·5% FCS. IGF-I displaced 125I-labelled IGF-I binding to serum IGFBPs with half-maximal inhibitory concentrations of approximately 1·5 nmol/1, while des(1–3)IGF-I and long R3 IGF-I only inhibited binding by 20% and 6% respectively, even at a concentration of 35 nmol/l. Similar affinities for IGF-I receptors on neutrophils and mononuclear cells were shown for IGF-I and des(1–3)IGF-I. Conversely, much lower affinities for these receptors were demonstrated for long R3 IGF-I. These results suggest that the biological activities of IGF-I and its analogues in cells of the bovine immune system depend on their binding characteristics both to receptors and to binding proteins.
Journal of Endocrinology (1993) 139, 259–265