• Zhiping Xie, Shaoxin Huang, Shenke Xie, Wu Zhou, Chengcai Li, Zelong Xing, Zhihua Wang, Zhiwu Wu, and Meihua Li.
• Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
• World Neurosurg. 2021 Oct 1; 154: e29-e38.

BackgroundDepression induced by spinal cord injury (SCI) has been demonstrated in clinical and experimental studies; it significantly impacts patients' lives and may be associated with changes in the hippocampus. However, the biological mechanisms underlying depression after SCI are unknown. The mitogen-activated protein kinase (MAPK) signaling pathway participates in potential mechanisms of depression; it is unknown whether this pathway plays a role in SCI-induced depression.MethodsWe applied an animal model of depression induced by SCI, established using an aneurysm clip, to determine whether MAPK activation in the hippocampus is associated with depression-like behavior.ResultsSCI led to depression-like behavior, such as anhedonia in the sucrose preference test, decreased number of crossings in the open field test, decreased body weight, and decreased immobility time in the forced swim test. Western blot analysis further showed that SCI significantly increased the levels of phosphorylated p38 MAPK and cleaved caspase-3 in the hippocampus and inhibited the phosphorylation of extracellular signal-related kinase 1/2 and c-Jun N-terminal kinase 1/2. In addition, there were significant negative correlations between depression-like behavior and phosphorylated extracellular signal-related kinase 1/2 and positive correlations between depression-like behavior and phosphorylated p38 MAPK and cleaved caspase-3.ConclusionsThese findings suggest that the MAPK pathway in the rat hippocampus may be involved in the pathophysiology of depression induced by SCI.Copyright © 2021 Elsevier Inc. All rights reserved.

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