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dc.creatorBotting, Shaleen Kaye
dc.date.accessioned2012-06-07T22:58:35Z
dc.date.available2012-06-07T22:58:35Z
dc.date.created2000
dc.date.issued2000
dc.identifier.urihttps://hdl.handle.net/1969.1/ETD-TAMU-2000-THESIS-B683
dc.descriptionDue to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.en
dc.descriptionIncludes bibliographical references (leaves 61-71).en
dc.descriptionIssued also on microfiche from Lange Micrographics.en
dc.description.abstractThe major relationship between ethanol and the behavioral response to environmental stressors indicates that ethanol functions to reduce the effects of stress. The most classical presentation of the anxiety-reduction hypothesis of alcoholism, presented by Cogner (1956), theorized that alcoholism was induced by the anxiolytic effects of ethanol, which in turn reinforced intake of ethanol. If this holds true, then it is reasonable to hypothesize that the CNS effects of ethanol may be dominant in the area of the brain that controls or influences anxiety. Given the known role of the amygdala in fear and anxiety-induced responses, we hypothesized that the anxiety reducing effects of ethanol would be observed within the amygdala and may be measured as alterations of neuronal excitability. The first aim of this thesis was to establish an animal model of alcoholism in the laboratory. This was done by introducing a nutritionally complete ethanol containing liquid diet. We compared two liquid diet formularies, one prepared in-house and one commercially prepared. The second aim enlisted a behavioral experiment to test our hypothesis of alterations of the anxiety response in the chronically ethanol treated rats. We utilized the light/dark box apparatus to measure the anxiolytic and anxiogenic effects of chronic ethanol ingestion and withdrawal. In these tests we found that both the ethanol and control rats displayed a slightly greater interest in exploring the dark side of the box, while the ethanol withdrawal rats spent a significant percent of their total time on the light side. The third aim was to use whole-cell patch clamp electrophysiology to study the cellular effects of ethanol on the rat basolateral amygdala neurons. Initially we were able to demonstrate that the acutely isolated BLA neurons contained strychnine-sensitive glycine receptors. However, we found no significant alteration in the glycine-, GABA-, or NMDA-mediated response within these neurons with chronic ethanol exposure or withdrawal.en
dc.format.mediumelectronicen
dc.format.mimetypeapplication/pdf
dc.language.isoen_US
dc.publisherTexas A&M University
dc.rightsThis thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries in 2008. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use.en
dc.subjectmedical sciences.en
dc.subjectMajor medical sciences.en
dc.titleThe effects of ethanol on strychnine sensitive glycine receptors in the rat basolateral amygdalaen
dc.typeThesisen
thesis.degree.disciplinemedical sciencesen
thesis.degree.nameM.S.en
thesis.degree.levelMastersen
dc.type.genrethesisen
dc.type.materialtexten
dc.format.digitalOriginreformatted digitalen


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