Date of Award

Spring 5-8-2017

Document Type

Thesis

Degree Name

Bachelor of Arts

Department

Nueroscience

First Advisor

Hewlet McFarlane

Abstract

Autism Spectrum Disorder is a neurodevelopmental disorder characterized by impairments in communication, social interaction deficits and repetitive, stereotyped, restricted behaviors (American Psychological Association, 2017). The BTBR T+tf/J (BTBR) is an inbred strain of mice that possesses several hallmark characteristics of Autism Spectrum Disorder, including aberrant social interactions and repetitive self-grooming (McFarlane et al., 2008). Additionally, BTBR mice have reduced inhibitory neurotransmission in comparison to their C57BL/6J (B6) counterparts (Han et al., 2014). The primary mediator of inhibitory neurotransmission in the brain is GABA acting on its receptors, primarily the GABAA subtype receptors. Previous studies have shown that agonism of the GABAA α2,3 subunits resulted in improvements in BTBR social approach (Han et al., 2014). The GABAA α2 receptor subunits are heavily localized in the hippocampus, striatum and the amygdala. The goal of this study is to examine if agonism of the GABAA2 receptor alone would result in the same improvements in sociability seen with the simultaneous agonism of the GABAA α2.

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