Neuroinflammatory priming to stress is differentially regulated in male and female rats

Publication date: May 2018Source: Brain, Behavior, and Immunity, Volume 70Author(s): Laura K. Fonken, Matthew G. Frank, Andrew D. Gaudet, Heather M. D'Angelo, Rachel A. Daut, Emma C. Hampson, Monica T. Ayala, Linda R. Watkins, Steven F. MaierAbstractExposure to stressors can enhance neuroinflammatory responses, and both stress and neuroinflammation are predisposing factors in the development of psychiatric disorders. Females suffer disproportionately more from several psychiatric disorders, yet stress-induced changes in neuroinflammation have primarily been studied in males. Here we tested whether exposure to inescapable tail shock sensitizes or ‘primes’ neuroinflammatory responses in male and female rats. At 24 h post-stress, male and female rats exposed to a peripheral immune challenge enhanced neuroinflammatory responses and exacerbated anxiety- and depressive-like behaviors. These changes are likely glucocorticoid dependent, as administering exogenous CORT, caused a similar primed inflammatory response in the hippocampus of male and female rats. Further, stress disinhibited anti-inflammatory signaling mechanisms (such as CD200R) in the hippocampus of male and female rats. In males, microglia are considered the likely cellular source mediating neuroinflammatory priming; stress increased cytokine expression in ex vivo male microglia. Conversely, microglia isolated from stressed or CORT treated females did not exhibit elevated cytokine responses. Microglia isolated fro...

Source: Brain, Behavior, and Immunity - July 10, 2018 Category: Neurology Source Type: research