Alicia Y Che, PhD

Project 1. The Role of Oxytocin on the Development of Social Behavior

Touch contributes powerfully to parent-infant interactions that are fundamental for early social behavior development. Abnormalities in tactile perception are prevalent features in individuals with autism spectrum disorders (ASD), exacerbating the core social deficits. While the neural mechanisms underlying the interplay between tactile input and social behavior is not yet known, a prominent route through which social information can be conveyed to neurons is oxytocin signaling. In neurons, oxytocin modulates inhibition to increase signal-to-noise ratios, promote long-term synaptic plasticity, and enhance the salience of socially-relevant stimuli. We are investigating how oxytocin facilitates the development of social touch on a circuit level. We use a combination of techniques including mouse genetics, slice electrophysiology, longitudinal in vivo 2-photon imaging on behaving animals to reveal how circuits underlying whisker-dependent social interaction is established.

Project 2. Circuit Dysfunction in PTSD

PTSD is a debilitating disorder involving intrusive memories of a traumatic events, which are due in part to an inability to modify responses to stimuli that are no longer threatening – a process known as extinction. The medial prefrontal cortex (mPFC) plays a critical role in extinction, however the circuit-level mechanisms that support extinction learning in the mPFC are not completely understood. Recent TWAS and gene expression studies on PTSD postmortem brain revealed numerous dysregulated genes expressed in GABAergic neurons in the dlPFC that are also key drivers capable of coordinating transcriptomic organization. We aim to understand how these genes are involved in fear extinction on cellular, circuit and functional levels with an emphasis on the developmental period, leveraging new technologies for cell type-specific genetic manipulations and 2-photon imaging through chronically implanted microprisms.