Mechanisms of Central IL-1 Responses to Stress

Suny At Binghamton, Binghamton NY

Investigators

Abstract

Exposure to stress leads to activation of multiple systems such as the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis, both of which evolved as endogenous mechanisms to promote survival in the face of diverse threats. However, considerably less attention has been devoted towards understanding brain mechanisms that promote functional recovery and adaptation after the threat subsides. As a result, we have argued that exposure to intense stressors requires a protracted period of recuperation, and that activation of inflammatory pathways in the brain as a result of stressor exposure promotes recuperative behavior. The goal of this project, therefore, is to determine the mechanisms by which stressor exposure leads to activation of inflammatory pathways in the brain. The researcher specifically hypothesizes that activation of central noradrenergic nuclei in response to stress are critical for activating these inflammatory pathways, while the release of corticosterone, the major effector molecule of the HPA axis in rat, constrains the development of neuroinflammation. In this regard, the project employs a systems biology approach that seeks to clarify the functional interplay among multiple stress responsive systems at the cellular, neurochemical, and neuroanatomical levels of analysis. The investigator's laboratory is comprised of trainees at all levels of the scientific hierarchy (undergraduates, graduate students and post doctoral trainees) and includes strong representation by underrepresented populations in the sciences (50% female, 33% minorities). The laboratory environment is state-of-the-art and contains extensive resources devoted specifically to promote training and networking for careers in science. The laboratory also has a strong history, and deliberate plans for, dissemination of findings to the scientific community (both domestic and abroad) as well as to the lay public.