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Estradiol exposure alters gonadothropin-releasing hormone (GNRH) induced gonadotrope plasticity

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dc.contributor.authorHartshorn, Cheryl, author
dc.contributor.authorTobet, Stuart, advisor
dc.contributor.authorClay, Colin, committee member
dc.contributor.authorHentges, Shane, committee member
dc.contributor.authorTjalkens, Ron, committee member
dc.date.accessioned2022-04-15T15:26:04Z
dc.date.available2022-04-15T15:26:04Z
dc.date.issued2010
dc.descriptionCovers not scanned.
dc.descriptionPrint version deaccessioned 2022.
dc.description.abstractThe reproductive axis is dependent upon communication among the hypothalamus, pituitary and gonads. For successful ovulation, a large increase in circulating estradiol provides positive feedback at both the hypothalamic and pituitary levels to promote an luteinizing hormone (LH) surge. An LH surge is necessary for the final maturation of the pre-ovulatory follicle and ovulation. The cellular and molecular events underlying estradiol’s action(s) upon the anterior pituitary gland, specifically gonadotropes, remain elusive. Recent video microscopy experiments showed that pituitary cells in vitro in slice culture move in response to GnRH [Navratil, et al., 2007]; presumably these cells were gonadotropes. The current study utilized a novel transgenic animal model that has gonadotrope specific fluorescence provided by yellow fluorescent protein (YFP) [Wen et al., 2008]. I sought to determine if 17(3-estradiol (E2) working through either a genomic or non-genomic mechanism affected gonadotrope specific movements in response to GnRH. Consistent with earlier studies [Navratil et al., 2007], application of GnRH [100nM] altered the cytoarchitecture of gonadotropes with observable cell process extensions. Using live video- microscopy, exposure to 10nM E2 for fourteen hours significantly enhanced the ability of gonadotropes to extend processes in response to GnRH compared to short-term exposure of E2 (1.5 hours) or vehicle. There was no demonstrable effect of 1.5 hours of E2 exposure on GnRH-induced process extensions. I hypothesize that the differential effect of short-term versus long-term E2 exposure is due to a genomic mechanism that may underlie the ability of E2 to enhance GnRH induced cellular plasticity. Thus, E2 and GnRH may cooperate to maximize the secretory interface between gonadotropes and the adjacent vasculature during the pre-ovulatory LH surge.
dc.format.mediummasters theses
dc.identifier.urihttps://hdl.handle.net/10217/234712
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relationCatalog record number (MMS ID): 991014244539703361
dc.relationQP572.L85 H378 2010
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subject.lcshEstradiol
dc.subject.lcshLuteinizing hormone releasing hormone
dc.titleEstradiol exposure alters gonadothropin-releasing hormone (GNRH) induced gonadotrope plasticity
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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