Replenishing what is Lost: Using Supplementation to Enhance Hippocampal Function in Fetal Alcohol Spectrum Disorders

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dc.contributor.authorPatten, Anna Ruth
dc.contributor.supervisorChristie, Brian R.
dc.date.accessioned2013-04-22T16:39:02Z
dc.date.copyright2013en_US
dc.date.issued2013-04-22
dc.degree.departmentProgram: Neuroscience
dc.degree.departmentDepartment of Biology
dc.degree.levelDoctor of Philosophy Ph.D.en_US
dc.description.abstractFetal Alcohol Spectrum Disorders (FASD) are the most common cause of cognitive impairment in the United States (Sokol et al., 2003). In young school children in North America and some Western European countries, recent reports have estimated the prevalence of FASD to be as high as 2-5% (May et al., 2009). Currently there are no widely accepted treatment options for FASD, mainly due to the fact that the underlying neurological deficits that occur with prenatal ethanol exposure (PNEE) are still largely unknown. This thesis examines the long-lasting changes that occur in the hippocampus following PNEE using biochemical and electrophysiological techniques. We find that PNEE produces a reduction of the endogenous antioxidant glutathione (GSH), resulting in an increase in oxidative stress that is accompanied by long-lasting reductions in long-term potentiation (LTP) of synaptic efficacy. Interestingly, males exhibited greater deficits in synaptic plasticity than females, despite similar reductions in GSH in both sexes. By depleting GSH in control animals we determined that LTP in the DG of female animals is more resistant to changes in GSH, which may explain the sexual dichotomy observed in these studies of PNEE. Based on these findings, ethanol-exposed animals received postnatal dietary supplementation with either a precursor of GSH, N-Acetylcysteine (NAC) or Omega-3 fatty acids. These supplements helped to counteract the effects of PNEE and improved hippocampal function. The findings in this thesis support the hypothesis that increasing antioxidant capacity can enhance hippocampal function, which in turn may improve learning and memory in FASD, providing a therapeutic avenue for children suffering with these disorders.en_US
dc.description.proquestcode0570 Nutritionen_US
dc.description.proquestcode0317 Neuroscienceen_US
dc.description.proquestemailanna.r.patten@gmail.comen_US
dc.description.scholarlevelGraduateen_US
dc.identifier.urihttp://hdl.handle.net/1828/4536
dc.languageEnglisheng
dc.language.isoenen_US
dc.rights.tempAvailable to the World Wide Weben_US
dc.subjectFetal Alcohol Spectrum Disordersen_US
dc.subjectPrenatal Ethanol Exposureen_US
dc.subjectElectrophysiologyen_US
dc.subjectDentate gyrusen_US
dc.subjectHippocampusen_US
dc.subjectOxidative Stressen_US
dc.subjectOmega-3 fatty acidsen_US
dc.subjectGlutathioneen_US
dc.titleReplenishing what is Lost: Using Supplementation to Enhance Hippocampal Function in Fetal Alcohol Spectrum Disordersen_US
dc.typeThesisen_US

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