- Browse by Subject
Browsing by Subject "Anxiolysis"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
Item Development, validation, and characterization of a novel preclinical animal model of social familiarity-induced anxiolysis(2017-09-29) Lungwitz, Elizabeth Ann; Shekhar, Anantha; Truitt, William; Oxford, Gerry; Rodd, Zachary; Lapish, ChristopherSocial support is a powerful therapeutic against fear and anxiety and is utilized in many psychotherapies. The concept that a familiar or friendly presence helps a person learn to overcome anxiety has been well-known for decades, yet, the basic neural mechanisms that regulate this psychosocial learning remain unknown. A first step towards elucidating these basic mechanisms is the development of a valid preclinical animal model. However, preclinical behavioral models exploring the use of a social presence in reducing anxiety have not been fully characterized. Therefore, it was our goal to identify a useful way in which to study the mechanisms of how a social presence can induce anxiolysis (the reduction of anxiety). We accomplished this goal by characterizing and validating a preclinical model, as well as demonstrating that the model was capable of measuring deficits in rats given a mild traumatic brain injury. To this end, we identified an existing, but uncharacterized model, the social interaction-habituation model, as an effective model of social familiarity-induced anxiolysis (SoFiA), which demonstrates socially enhanced safety learning, or psychosocial learning. We find that as social familiarity develops across time, anxiolysis develops. We identified that the use of a Bright Light Challenge is a useful anxiogenic stimulus to use during SI-habituation training. The anxiolysis acquired following SI-habituation testing is partner specific, and can be blocked by an inhibition of the medical prefrontal cortex, while it can be enhanced by D-cycloserine. We found that this model identified deficits in SoFiA acquisition in rodents exposed to a mild traumatic brain injury, which, in humans, has been linked to psychosocial deficits. This work is a step in creating ways in which we can study and better understand the regulatory processes of emotions mediated by social behavior.Item Identifying the Neural Circuit That Regulates Social Familiarity Induced Anxiolysis (SoFiA)(2020-06) Majumdar, Sreeparna; Cummins, Theodore R.; Truitt, William A.; Block, Michelle L.; Johnson, Phillip L.; Engleman, Eric A.Mental health is crucially linked to social behavior. A crucial aspect of healthy social behavior involves learning to adapt emotional responses to social cues, for example learning to suppress anxiety through social familiarity, or social familiarity induced anxiolysis (SoFiA). SoFiA is well documented; however, the neural mechanisms of SoFiA are unclear. SoFiA is modeled in rats by employing a social interaction habituation (SI-hab) protocol. Using SI-hab protocol it has been determined that SoFiA represents social safety learning, which requires both anxiogenic stimulus (Anx) and social familiarity (SF) during training sessions (5-6 daily SI sessions), and SoFiA expression is dependent on infralimbic cortex (IL). Based on these findings we hypothesize that Anx and SF are processed by unique neural systems, and repeated convergence of these signals interact within IL to induce plasticity, resulting in social safety learning and anxiolysis. Following SoFiA expression, rats were either sacrificed 30 minutes {for gene expression or Neural Activity Regulated Gene (NARG) analysis} or perfused 90 minutes (for cFos immunoreactivity analysis) after SI session on social training day 5. This led to gaining insights into regions of brain involved in SoFiA response as well as the underlying molecular mechanisms. We identified amygdala, specifically the central amygdala (CeA), basomedial amygdala (BMA) and basolateral amygdala (BLA) as potential candidate regions in SoFiA response. Next, we investigated the role of IL and its efferent pathways in SoFiA expression using inhibitory DREADDs and intersectional chemogenetics to inhibit IL projection neurons and/or axons. We identified that specific projection neurons within the IL are pivotal for SoFiA expression, and that within these projections, the ones that specifically projected to the amygdala are most crucial for expression of SoFiA.