Developmental Alterations in Inhibitory Neurotransmission in the Fragile X Syndrome Mouse Basolateral Amygdala

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dc.contributor.advisorCorbin, Joshua Gen_US
dc.contributor.authorKratovac, Sebilaen_US
dc.contributor.departmentBiologyen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2013-02-07T07:18:40Z
dc.date.available2013-02-07T07:18:40Z
dc.date.issued2012en_US
dc.description.abstractFragile X Syndrome, caused by Fmr1 gene inactivation, is characterized by symptoms including enhanced fear, hyperactivity, social anxiety, and autism, pointing to synaptic and neural circuit defects in the amygdala. Previous studies in Fmr1 knockout (KO) mice have demonstrated alterations in GABAA receptor (GABAAR) function in the basolateral amygdala during early postnatal development. In this study, we sought to determine whether these early defects in GABAAR function are accompanied by changes in protein expression of GABAAR alpha 1, 2, and 3 subunits, the pre-synaptic GABA-synthesizing proteins GAD65 and 67 (GAD65/67), and the post-synaptic GABAAR-clustering protein gephyrin. We found that the developmental trajectory of protein expression is altered in knockout mice for all tested proteins except GABAAR alpha 3 and GAD 65/67. Our results suggest that alterations in the timing of inhibitory synapse protein expression in early postnatal development could contribute to observed inhibitory neurotransmission deficits in the KO mouse basolateral amygdala.en_US
dc.identifier.urihttp://hdl.handle.net/1903/13650
dc.subject.pqcontrolledNeurosciencesen_US
dc.subject.pqcontrolledDevelopmental biologyen_US
dc.subject.pqcontrolledBiologyen_US
dc.subject.pquncontrolledamygdalaen_US
dc.subject.pquncontrolledanxietyen_US
dc.subject.pquncontrolledautismen_US
dc.subject.pquncontrolleddevelopmenten_US
dc.subject.pquncontrolledFragile X Syndromeen_US
dc.subject.pquncontrolledinhibitory synapseen_US
dc.titleDevelopmental Alterations in Inhibitory Neurotransmission in the Fragile X Syndrome Mouse Basolateral Amygdalaen_US
dc.typeThesisen_US

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