Postoperative cognitive deficits and neuroinflammation in the hippocampus triggered by surgical trauma are exacerbated in aged rats

Abstract Postoperative cognitive dysfunction (POCD) is characterized by the progressive deterioration of intellectual/cognitive function following surgery. It has been suggested that the senile brain, which characteristically expresses higher levels of central proinflammatory cytokines, interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α, is more susceptible to additional insult following surgery. The authors of this study investigated the expression of central cytokines IL-1β, IL-6 and TNF-α and hippocampal glial cell activation in aged and adult rats following partial hepatectomy. Cognitive function was assessed in a reversal-learning version of the Morris water maze (MWM) before and after surgery. Hippocampal pro-inflammatory cytokines IL-1β, IL-6 and TNF-α and glial cell activation markers glial fibrillary acidic protein (GFAP) and S100β were measured at each time point; CD200 and CD200R were also measured to explore potential mechanisms of glial cell activation. Surgical trauma resulted in impairments in distance and latency only on postoperative day 1 (p  Overall, these findings suggest that surgical trauma, rather than anesthesia, resulted in cognitive function impairment potentiated by aging. Hippocampal pro-inflammatory cytokines and glial cell activation might mediate trauma-induced POCD.