Talk abstracts
Talk on Wednesday 09:45-10:00am submitted by Anzela Niraula
Repeated Social Defeat Stress Induces Neuroinflammation and Impairs Hippocampal Neurogenesis That Differentially Regulate Mood and Cognition
Anzela Niraula (Neuroscience Graduate Program), Daniel B. McKim (Neuroscience Graduate Program), Andrew J. Tarr (Oral Biology), Eric S. Wohleb (Neuroscience Graduate Program), John Sheridan (Oral Biology), Jonathan Godbout (Neuroscience Graduate Program)
Abstract:
Repeated social defeat (RSD) is a murine stressor that models several key physiological, immunological, and behavioral alterations observed in humans exposed to psychosocial stress. RSD induces prolonged anxiety-like behavior associated with myeloid cell trafficking into the brain, including the hippocampus - a key area involved in neuroplasticity, behavior, and cognition. Therefore, the goal of this study was to investigate if the stress-induced monocyte trafficking affected hippocampal neurogenesis and cognitive function. Here, we show that RSD increased inflammatory mediators (IL1b, TNFa and IL-6) in the hippocampus, and enhanced microglia activation and monocyte trafficking (CD45hi) specifically in the caudal hippocampus. RSD also impaired spatial memory recall in the Barnes maze independent of anxiety-like behavior. RSD did not affect the number of proliferating neural progenitor cells and developing neurons when examined 14 hours post-RSD. However, there was a significant reduction in the number of young neurons and mature neurons when examined 10 days and 28 days post-RSD respectively. Consistent with region-specific neuroinflammation, reduction in the number of mature neurons was greater in the caudal hippocampus of the RSD mice compared to controls. The RSD-induced spatial deficits, which are rostral hippocampus-mediated, were resolved by 28 days. Social avoidance which is caudal hippocampus-mediated still persisted 28 days after stress. Thus, stress-induced neuroinflammation is associated with reduced neuroplasticity, and the stress-induced affective and cognitive deficits are differentially associated with hippocampal neurogenesis.
Keywords: neurogenesis, macrophages, stress