Postdoctoral Scholar/ Colbran Lab
It is well established that Ca2+/calmodulin dependent protein kinase II alpha (CaMKII alpha) is important for synaptic plasticity, learning and memory. Mutations in the CAMK2A gene, which encodes CaMKII alpha, have been linked to Autism Spectrum Disorder (ASD) and intellectual disability. Previous characterization of mice harboring an ASD-associated Glu183 to Val knock-in mutation in CaMKII alpha (E183V-KI), which reduces CaMKII alpha expression and activity, revealed an impairment in social motivation, increased repetitive behaviors, as well as hyperactivity. Thus, I am interested in understanding the underlying sensory deficits that contribute to social impairments in E183V-KI mice.