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Ethanol 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 disorder

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Please use this identifier to cite or link to this item: http://hdl.handle.net/1928/20866

Ethanol 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 disorder

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Title: Ethanol 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 disorder
Author: Puglia, Michael
Advisor(s): Valenzuela, Carlos Fernando
Committee Member(s): Partridge, Don
Shuttleworth, Bill
Mueller, Wolfgang
Department: University of New Mexico. Biomedical Sciences Graduate Program
Subject(s): ethanol
development
plasticity
glutamate
syanptic
LC Subject(s): Fetal alcohol syndrome.
Alcohol--Pathophysiology.
Neurotoxicology.
Neural transmission.
Neuroplasticity.
Glutamic acid.
Hippocampus (Brain)
Degree Level: Doctoral
Abstract: Fetal 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.
Graduation Date: May 2012
URI: http://hdl.handle.net/1928/20866

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