Please use this identifier to cite or link to this item: http://hdl.handle.net/10125/62301

Juvenile Shank3b Deficient Mice Present With Behavioral Phenotype Consistent With Autism Spectrum Disorder

File Size Format  
2017-12-ms-balaan.pdf 1.06 MB Adobe PDF View/Open

Item Summary

Title:Juvenile Shank3b Deficient Mice Present With Behavioral Phenotype Consistent With Autism Spectrum Disorder
Authors:Balaan, Chantell
Contributors:Developmental & Reprod Biology (department)
Keywords:Shank3b
Autism Spectrum Disorder
Mouse Behavior
Date Issued:Dec 2017
Publisher:University of Hawaiʻi at Mānoa
Abstract:Autism spectrum disorder (ASD) is a pervasive, multifactorial neurodevelopmental disorder diagnosed according to deficits in three behavioral domains: communication, social interaction, and stereotyped/repetitive behaviors. Mutations in Shank genes account for ~1% of clinical ASD cases with Shank3 being the most common gene variant. In addition to maintaining synapses and facilitating dendritic maturation, Shank genes encode master scaffolding proteins that build core complexes in the postsynaptic densities of glutamatergic synapses. Male mice with a deletion of the PDZ domain of Shank3 (Shank3B KO) were previously shown to display ASD-like behavioral phenotypes with reported self-injurious repetitive grooming and aberrant social interactions. Our goal was to extend these previous findings and use a comprehensive battery of highly detailed ASD-relevant behavioral assays including an assessment of mouse ultrasonic communication carried out on key developmental days in male and female Shank3B KO mice. We demonstrate that ASD-related behaviors, atypical reciprocal social interaction and indiscriminate repetitive grooming, are apparent in juvenile stages of development of Shank3B KO mice. Our findings underscore the importance of utilizing Shank mutant models to understand the impact of this gene in ASD etiology, which may enable future studies focusing on etiological gene-environment interactions in ASD.
Description:M.S. Thesis. University of Hawaiʻi at Mānoa 2017.
URI:http://hdl.handle.net/10125/62301
Rights:All UHM dissertations and theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission from the copyright owner.
Appears in Collections: M.S. - Developmental and Reproductive Biology


Please email libraryada-l@lists.hawaii.edu if you need this content in ADA-compliant format.

Items in ScholarSpace are protected by copyright, with all rights reserved, unless otherwise indicated.