An optogenetic dissection of the role of the prelimbic cortex in subserving social behavior

Abstract

The goal of this thesis is to determine how optogenetic disruption of specifics components of neural circuits thought to underlie social behavior alters this behavior in mice. Social behavior has long been an area of interest for researchers, but the current literature still lacks a clear image of the cell-type specific circuitry and circuit dynamics that subserve it. Moreover, while abundant research has been conducted at the circuits and systems level on sexual, adolescent, and pathological social behavior, not much is known about the specifics of adult, same-sex non-aggressive interaction – arguably a category that most matches what is considered standard social behavior. In this thesis, we focused on the prefrontal cortex and its projections, as activity in the region has often been implicated in various social behaviors. We targeted the prelimbic cortex within the prefrontal cortex, as it projects to more limbic downstream areas that are likely to be involved in social processes. Using optogenetics, we stimulated projections from the prelimbic cortex (PL) to the nucleus accumbens (NAc), ventral tegmental area (VTA), and basolateral amygdala, and analyzed how this affect mouse behavior in a social task. We found that the PL \(\to\) NAc projection caused a decrease in social behavior when disrupted, corresponding to in vivo calcium imaging correlates that Malavika Murugan of the Witten Lab recently discovered. Surprisingly, we also found that stimulating PL \(\to\) VTA neurons causes increased movement velocity, producing a double dissociation of PL \(\to\) NAc and PL \(\to\) VTA function. Our long-term goal is to pair these optogenetic screenings of circuit function with in vivo calcium imaging neural correlate data to map the neural circuitry supporting all social behaviors.