Exploratory Study of Deep Brain Stimulation in the Syngap1+/- Mouse Model of Autism Spectrum Disorder Using Electrophysiology
Abstract
Syngap1+/- haploinsufficiency is phenotypically characterized by autism spectrum disorder (ASD), intellectual disability (ID), and epilepsy. SynGAP (Synaptic Ras GTPase-activating protein) is a protein that regulates function in synapses. In addition, SynGAP protein is an integral component of the post-synaptic density and its role in signaling pathway converges with other autism risk genes and consequently autism risk proteins. A critical gap exists to understand how electrical stimulation as part of the Hebbian theory, can induce neuroplasticity. Previously, success in alleviating self-injurious behavior along with facilitating speech formation was demonstrated in adolescent patients undergoing deep brain stimulation (DBS) of the basolateral amygdala (BLA). Therefore, we sought to develop a chronic DBS model in Syngap1+/- haploinsufficient mice that can be used to assess the behavior and proteomic correlates due to DBS in BLA.
Degree
M.Eng.
Advisors
Kinzer-Ursem, Purdue University.
Subject Area
Neurosciences
Off-Campus Purdue Users:
To access this dissertation, please log in to our
proxy server.