| dc.description.abstract | All organisms are united by the need to respond to environmental pressures, or stress. The response to stress initiates a biological cascade that attempts to facilitate a reconciliation of the stressor, either through escape or confrontation. This response occurs in numerous forms, but in instances of a repeated psychosocial stressor, there is a specific set of psychological and physiological changes can arise. However, recent evidence suggests that in addition to reconciliation, the response to a repeated stressor also facilitates biological changes that can prime the immune system to respond to immunological threats with an exacerbated response. While adaptive, activation of the immune systems inflammatory response has also been linked to the genesis and progression of numerous diseases. Specifically, research within our lab has demonstrated a link between repeated bouts of immune activation and the production of amyloid-ß (Aß), the protein associated with plaques of Alzheimers disease. The following data presents support for the hypothesis that repeated stress followed by repeated activation of the immune system elevate hippocampal Aß and induce significant cognitive deficits. We also demonstrate that administration of glycyrrhizin prior to and immediately after the experience of stress can prevent the stress-induced alterations in the immune response. Additionally, we show that the inflammatory response within the dorsal and ventral hippocampus interacts with repeated stress, such that stress alters the regional expression of IL-1ß and HMGB1 mRNA. Cumulatively, previous data with our lab, combined with the present experiments, demonstrate that repeated stress can exaggerate an induced immune response, potentiate sickness behaviors, elevate the accumulation of inflammatory induced Aß, and create regionally distinct patterns of immune activation within the hippocampus. | |
