Date of Award:

5-1-1991

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Biology

Department name when degree awarded

Biology (Endocrinology)

Committee Chair(s)

LeGrande C. Ellis

Committee

LeGrande C. Ellis

Committee

Warren C. Foote

Committee

Jay W. Call

Committee

Reed P. Warren

Committee

James A. Gessaman

Abstract

This study was designed to investigate the hypothalamic-pituitary-testicular axis of the primary infertile dark male mink. The specific objectives were (1) to describe the morphology and localization of the neurons containing gonadotropin-releasing hormone (GnRH) and its precursor (proGnRH) within the preoptic-basal hypothalamus (POA-BH) of the sexually mature dark male mink, (2) to ascertain any differences in the number or the distribution of GnRH- and proGnRH-containing neurons between the fertile and infertile dark male mink, (3) to determine if GnRH and proGnRH are produced in insufficient amounts by the hypothalami of primary infertile dark male mink, and (4) to describe the microscopic changes in the pituitary and testis of primary infertile dark mink and identify any histological changes that might contribute to their abnormal functions. The severity of the microscopic morphologic changes of the pituitary glands and testes of infertile mink were evaluated and scaled both quantitatively and semi-quantitatively. Accordingly, two forms were identified: (1) those with hypoplastic testes and microcystic degeneration of the pituitary glands (infertile group I), and (2) those with degenerative testicular changes but normal pituitary glands (infertile group II). GnRH- and proGnRH-containing neurons were found in the POA, the organum vasculosum of the lamina terminalis, and in the anterior hypothalamus, lateral to the suprachiasmatic nucleus. They were abundant in the infundibular area of the hypothalamus, mainly the median eminence. More GnRH, but not proGnRH, immunoreactive neurons were found in the rostral basal hypothalamus than in the suprachiasmatic nucleus (P < 0.05) in the control and infertile group II, but not in the infertile group I mink. No differences were found in the general morphology or localization of the immunoreactive GnRH and proGnRH neurons, or their immunoreactive levels in the various POA-BH regions across the mink groups. The data indicate that the two forms of primary infertility in dark mink identified in this study are caused by different endocrinologic abnormalities: (1) the testicular hypoplasia in infertile group I mink is probably related to an innate defect in the pituitary gland, and (2) the testicular degeneration in infertile group II mink is not due to failure of developmental migration of GnRH neurons to the POA-BH, nor due to defect in GnRH synthesis or number of GnRH- or proGnRH-containing neurons in the POA-BH. We speculate that it may be due to delayed activation of GnRH secretion.

Download

Share

COinS

Copyright for this work is retained by the student. If you have any questions regarding the inclusion of this work in the Digital Commons, please email us at .