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dc.contributor.authorPuglia, Michael
dc.date.accessioned2012-07-05T22:10:50Z
dc.date.available2012-07-05T22:10:50Z
dc.date.issued2012-07-05
dc.date.submittedMay 2012
dc.identifier.urihttp://hdl.handle.net/1928/20866
dc.description.abstractFetal alcohol spectrum disorder results from developmental exposure to ethanol. Although many organ systems are targeted by this teratogen, the central nervous system is exquisitely sensitive. Children with this disease often present with behavioral disorders as well as impairments in learning and memory. Ethanol exposure affects developmental processes throughout pregnancy; however, the third trimester-equivalent has demonstrated heightened sensitivity. Although the mechanism of action(s) of ethanol remains unknown, studies suggest that impairments in glutamatergic signaling and synaptic plasticity during the third trimester-equivalent period of development lead to alterations in synaptic formation and refinement. However, little is known about the developmental effects of ethanol in the CA1 hippocampal region, a brain region often studied in the context of learning and memory. Studies presented in this dissertation address the acute and chronic effects of ethanol during the third trimester-equivalent period. First, characterization of the acute effects of ethanol demonstrated postsynaptic inhibition of both NMDA receptor (NMDAR) and AMPA receptor (AMPAR) mediated synaptic responses, as well as the inhibition of long-term potentiation (LTP) induction. Then, an in vivo repeated ethanol exposure paradigm was used to mimic maternal drinking during this period. In contrast to the effects of acute ethanol exposure, repeated exposure did not affect AMPAR- or NMDAR-mediated synaptic strength or glutamate release; however, it impaired LTP expression and/or maintenance. Lastly, repeated in vivo third trimester-equivalent ethanol exposure did not affect expression of Ca2+-permeable AMPARs, or induce tolerance to the acute inhibitory effects of ethanol. Studies in this dissertation add to a growing body of evidence indicating that significant differences exist between the effects of ethanol on the developing versus the mature brain. Furthermore, studies presented here support the notion that ethanol-mediated impairments in synaptic plasticity mechanisms during the third trimester-equivalent developmental period could lead to inappropriate wiring of neuronal circuitry, and set the stage for the long term deficits observed in children with fetal alcohol spectrum disorder.en_US
dc.description.sponsorshipNational Institute on Alcohol Abuse and Alcoholism, University of New Mexico MD/PhD Programen_US
dc.subjectethanolen_US
dc.subjectdevelopmenten_US
dc.subjectplasticityen_US
dc.subjectglutamateen_US
dc.subjectsyanpticen_US
dc.subject.lcshFetal alcohol syndrome.
dc.subject.lcshAlcohol--Pathophysiology.
dc.subject.lcshNeurotoxicology.
dc.subject.lcshNeural transmission.
dc.subject.lcshNeuroplasticity.
dc.subject.lcshGlutamic acid.
dc.subject.lcshHippocampus (Brain)
dc.titleEthanol exposure impairs glutamatergic synaptic transmission and plasticity in the ca1 hippocampal region during the third trimester-equivalent of human pregnancy : implications for fetal alcohol spectrum disorderen_US
dc.typeDissertationen_US
dc.description.degreeBiomedical Sciencesen_US
dc.description.levelDoctoralen_US
dc.description.departmentUniversity of New Mexico. Biomedical Sciences Graduate Programen_US
dc.description.advisorValenzuela, Carlos Fernando
dc.description.committee-memberPartridge, Don
dc.description.committee-memberShuttleworth, Bill
dc.description.committee-memberMueller, Wolfgang


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