PGE2-EP3 signaling exacerbates hippocampus-dependent cognitive impairment after laparotomy by reducing expression levels of hippocampal synaptic plasticity-related proteins in aged mice

CNS Neuroscience & Therapeutics
Jing-Yu XiaoYu-Ke Tian

Abstract

Multifactors contribute to the development of postoperative cognitive dysfunction (POCD), of which the most important mechanism is neuroinflammation. Prostaglandin E2 (PGE2) is a key neuroinflammatory molecule and could modulate hippocampal synaptic transmission and plasticity. This study was designed to investigate whether PGE2 and its receptors signaling pathway were involved in the pathophysiology of POCD. Sixteen-month old male C57BL/6J mice were exposed to laparotomy. Cognitive function was evaluated by fear conditioning test. The levels of PGE2 and its 4 distinct receptors (EP1-4) were assessed by biochemical analysis. Pharmacological or genetic methods were further applied to investigate the role of the specific PGE2 receptors. Here, we found that the transcription and translation level of the EP3 receptor in hippocampus increased remarkably, but not EP1, EP2, or EP4. Immunofluorescence results showed EP3 positive cells in the hippocampal CA1 region were mainly neurons. Furthermore, pharmacological blocking or genetic suppression of EP3 could alleviate surgery-induced hippocampus-dependent memory deficits and rescued the expression of plasticity-related proteins, including cAMP response element-binding protein (CREB), ac...Continue Reading

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Citations

Mar 10, 2020·Oxidative Medicine and Cellular Longevity·Yuen-Shan HoRaymond Chuen-Chung Chang
Nov 26, 2019·Experimental Gerontology·Xianyi LinXin Yu
Aug 2, 2020·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Paula MoyanoJavier Del Pino
Jan 7, 2022·CNS Neuroscience & Therapeutics·Yang LiuTianlong Wang

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