Poster Session II
Project Type
Poster
Faculty Mentor’s Full Name
Andrew Rau
Faculty Mentor’s Department
Neuroscience
Abstract / Artist's Statement
Post-traumatic stress disorder (PTSD) is a debilitating neuropsychiatric disorder that affects diverse populations across the United States. First-line treatments, including selective serotonin reuptake inhibitors (SSRIs) and psychotherapy, are often only partially effective. Although novel therapeutic strategies are emerging, the neurobiological mechanisms underlying both PTSD and its treatment remain poorly understood. To advance the development of more effective interventions, it is essential to define the cellular and circuit-level mechanisms that govern traumatic memory storage. The medial prefrontal cortex (mPFC) plays a critical role in fear learning and memory. However, how specific neuronal populations, particularly interneurons, are altered by fear learning remains unclear. To determine whether fear memory encoding recruits mPFC somatostatin (SST) interneurons, we used immunohistochemistry to quantify c-Fos expression in SST-positive cells 24 hours after cued fear conditioning. Fear-conditioned mice exhibited increased colocalization of SST interneurons with c-Fos, indicating enhanced activation of mPFC SST cells following fear learning. In addition to increased activity, mPFC SST interneurons displayed greater dendritic spine density and a higher proportion of mature, mushroom-shaped spines compared to controls, suggesting that fear learning strengthens excitatory synaptic input onto these cells. Notably, mPFC SST interneurons express GluN3A-containing NMDA receptors, which are implicated in dendritic spine development and synaptic plasticity. Prior studies have shown that GluN3A knockout mice exhibit impairments in fear extinction, implicating GluN3A signaling in the regulation of fear-related circuitry. Together, these findings suggest that GluN3A expression in mPFC SST interneurons may contribute to the synaptic and circuit adaptations that support fear learning and extinction.
Category
Life Sciences
Fear Conditioning Enhances Activity and Synaptic Maturation of mPFC Somatostatin Interneurons
UC South Ballroom
Post-traumatic stress disorder (PTSD) is a debilitating neuropsychiatric disorder that affects diverse populations across the United States. First-line treatments, including selective serotonin reuptake inhibitors (SSRIs) and psychotherapy, are often only partially effective. Although novel therapeutic strategies are emerging, the neurobiological mechanisms underlying both PTSD and its treatment remain poorly understood. To advance the development of more effective interventions, it is essential to define the cellular and circuit-level mechanisms that govern traumatic memory storage. The medial prefrontal cortex (mPFC) plays a critical role in fear learning and memory. However, how specific neuronal populations, particularly interneurons, are altered by fear learning remains unclear. To determine whether fear memory encoding recruits mPFC somatostatin (SST) interneurons, we used immunohistochemistry to quantify c-Fos expression in SST-positive cells 24 hours after cued fear conditioning. Fear-conditioned mice exhibited increased colocalization of SST interneurons with c-Fos, indicating enhanced activation of mPFC SST cells following fear learning. In addition to increased activity, mPFC SST interneurons displayed greater dendritic spine density and a higher proportion of mature, mushroom-shaped spines compared to controls, suggesting that fear learning strengthens excitatory synaptic input onto these cells. Notably, mPFC SST interneurons express GluN3A-containing NMDA receptors, which are implicated in dendritic spine development and synaptic plasticity. Prior studies have shown that GluN3A knockout mice exhibit impairments in fear extinction, implicating GluN3A signaling in the regulation of fear-related circuitry. Together, these findings suggest that GluN3A expression in mPFC SST interneurons may contribute to the synaptic and circuit adaptations that support fear learning and extinction.