Postdoctoral Scholar, Calipari Lab
The main goal of my research has been to elucidate the genetic mechanisms underlying sex differences in behavioral strategies and learning that may influence differences in several mental health diseases including depression and addiction. Toward this end, I did experiments that have included a reward learning procedure followed by proteomics in the nucleus accumbens in both male and female mice. I also performed experiments that elucidated a role for the estrous cycle in cue learning and correlated reinstatement with cfos expression in the striatum.
Postdoctoral Scholar, Broadie Lab
I am researching the molecular and cellular function of Fragile X Mental Retardation Protein (FMRP), loss of which results in Fragile X syndrome (FXS), the most common heritable cause of autism spectrum disorder and intellectual disability. I model the disease state in Drosophila, working on conserved molecular machinery in the central brain learning and memory circuitry. I am focusing my investigations on activity-dependent signaling, cytoskeleton regulation and synapse formation/refinement. My aim is to dissect causes of and solutions for genetic sources of autism spectrum disorder and intellectual disability.
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.