Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 91-102). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 91-102). Also available on the Internet.

Factors influencing testicular gonadotropin receptors and testis responsiveness to luteinizing hormone (LH) stimulation were studied during the seasonal sexual cycle of the adult ram. The normal variation in testis content of gonadotropin receptors was mapped out in relation to changes in (1) testis size, (2) testis responsiveness to LH stimulation and (3) mean serum concentration of LH, follicle stimulating hormone (FSH), testosterone and prolactin (PRL). The increase in gonadotropin receptor numbers during testicular redevelopment was preceded by elevated serum concentrations of PRL and associated with increases in both the frequency of endogenous pulses of LH and the responsiveness of the testis to LH stimulation. When serum PRL concentrations displayed abnormal variations in relation to photoperiod, the normal patterns of change in testis LH receptors and responsiveness to LH stimulation were altered. To determine if the increase in gonadotropin receptors was due to increased frequency of LH pulses up regulating homologous receptors, rams were injected, in the nonbreeding season with small, frequent doses of LH. Testis responsiveness was greatly enhanced but occurred independently of changes in gonadotropin receptor numbers or their binding affinities. To determine if the seasonal rise in serum PRL concentration was influencing gonadotropin receptors, endogenous secretion was suppressed by treatment with 2-bromo-X-ergocryptine (CB154) prior to and during testicular redevelopment. This resulted in delayed testicular redevelopment and reduced numbers of testicular LH receptors. Reduced numbers of LH receptors was associated with reduced responsiveness of the testis to LH stimulation. These results support the hypothesis that the seasonal increase in serum PRL concentration initiates testicular redevelopment by increasing LH receptors. Increases in LH peak frequency enhance responsiveness but this occurs independently of changes in gonadotropin receptors.

Thesis (Ph.D.) -- University of Adelaide, Department of Obstetrics and Gynaecology, 1981.

Zugl.: Giessen, Universiẗat, Diss., 2007.

Zugl.: Giessen, Universiẗat, Diss., 2007.

Thesis (M.N.A.S.)--Missouri State University, 2008. / "May 2008." Includes bibliographical references (leaves 43-47). Also available online.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Superovulatory treatment with exogenous gonadotrophins adversely affects the uterus through the disruption of the delicate balance of ovarian steroid (estrogens, progestins, androgens) secretion rates. To examine the uterine effects of this treatment, 189 animals were given 4, 20 or 40 IU pregnant mare serum gonadotrophin (PMSG) at 28 days of age and sacrificed every 24 h until day 10 (D10) post injection. To study the long term uterine effects, 12 rats were treated with 4 or 40 IU PMSG and killed on D30. The morphological and histological changes of control (4 IU) uteri mimicked those of the adult on a comparable time course from D2 to D5. Administration of superovulatory doses (2 0, 4 0 IU) of PMSG produced stromal hypertrophy by D2 and focal papillary hyperplasia of the luminal epithelia by D3. It is suggested that previous exposure to high levels of estrogen and androgens, secondary to superovulation, are possible causes for this pathology. Levels of 17B-estradiol following 2 0 and 40 IU PMSG treatment were significantly (p<0.005, p<0.05) elevated above those of controls from DI to early D3 and at D2, respectively. Androgen levels of both groups (20 IU, 40 IU) significantly (p<0.05, p<0.005) increased from baseline at DI to maxima by D2 and D3, respectively. In the 20 IU PMSG group, the hyperplasia gradually regressed after D3 and was absent by D10. The hyperplasia in the 40 IU PMSG group, however, had diffused by D6. It is suspected that preceding elevated levels of estrogen may be responsible for this progressive change. At D4, levels of 17B-estradiol reached a maximum, which was significantly (p<0.001) greater than those of controls and 20 IU PMSG treated rats. Between D6 and D10, the hyperplasia partially regressed. Examination of uteri from D30 revealed no evidence of pathology. In addition to these structural effects, superovulation induced secretion of a mucinous substance in both 20 IU and 40 IU PMSG groups at D5-D6 and D6-D7, respectively. These results suggest that abnormal changes in the uterine histology and metabolism may result following administration of superovulatory doses of PMSG. Although these dose-dependent alterations appear reversible, they may interfere with preparations associated with implantation and thus require further investigation. / Medicine, Faculty of / Obstetrics and Gynaecology, Department of / Graduate

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