B31: The Effects of Acute Early Life Stress and Social Buffering on Anxiety Behavior, Corticosterone Secretion, and Receptor Protein Expression in Adulthood

Although the psychopathological impacts of stress are far-reaching, the mechanisms of these consequences remain poorly understood. Recent evidence implicates a social component in the development of stress-induced psychopathologies. The presence of a social partner can ameliorate the consequences of stress exposure, a phenomenon known as social buffering. To better understand this phenomenon, this study sought to determine whether the effects of acute early life stress (ELS) would be impacted by subsequent exposure to social buffering (SB) or isolation. A growing body of literature implicates corticotropin-releasing hormone (CRH) and serotonergic (5-HT) receptors in the long-term outcomes of ELS exposure. We hypothesized that exposure to acute ELS would increase anxiety behavior and anxiety-induced corticosterone secretion in adulthood based on this evidence. We hypothesized that social buffering would ameliorate these effects. We exposed mouse pups to a context chamber on prenatal day 17 (PND17) to test our hypotheses. Mouse pups were randomly assigned to the no ELS (0 footshocks) or ELS (15 footshocks) conditions. Following the chamber experience, mouse pups were randomly assigned to either SB or isolation. On PND60, we measured anxiety-like behaviors in the adult mice by employing an open field test (OFT). Upon completion of the OFT, mice were sacrificed, and their plasma corticosterone levels were collected and analyzed. Mouse brains were collected and dissected to examine CRH2 and 5-HT2C receptor expression in specific brain regions (BNST, CeA, and DRN). Ongoing analyses will quantify the expression of these proteins. Our behavioral results indicate that mice subjected to ELS did not exhibit more anxiety-like behavior than mice that did not experience the stressor. Moreover, social buffering did not reduce the effects of ELS. Such evidence reinforces a second-hit model of the etiology of psychopathological disorders, in which a single stress exposure produces a “vulnerable” rather than a pathological organism.

Authors: Chelsea Worrell, Shannon Seabolt, Brynne Menkhaus

Advisor: Jennifer Quinn, Psychology

Graduate Advisor: Amanda Reichert, Psychology

Related Posts

Begin typing your search term above and press enter to search. Press ESC to cancel.

Back To Top