• C-Q Wang, Y Ye, F Chen, W-C Han, J-M Sun, X Lu, R Guo, K Cao, M-J Zheng, and L-C Liao.
• College of Basic and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China; Department of Pathology, Xuzhou Medical College, Xuzhou, Jiangsu 221004, China.
• Neuroscience. 2016 Dec 1.

AbstractAs a complex disease, traumatic brain injury (TBI) can result in long-term psychiatric changes and sensorimotor and cognitive impairments. The TBI-induced loss of memory and long-term cognitive dysfunction are related to mechanistic factors including an increased inflammatory response, autophagy, edema, and ischemia. Many published studies have offered evidence for the neuroprotective effects and anti-inflammatory properties of ketamine for TBI patients. Nonetheless, there is a limited understanding of the accurate mechanism that underlies the potential neuroprotective effects of ketamine. Herein, it can be shown that posttraumatic administration of ketamine at a sub-anesthetic dose (10mg/kg ketamine, every 24h up to 7days) can prevent the TBI-induced production of IL-6 and TNF-α, attenuate deficits of dendrites and spines and exert beneficial effects on memory and behavior. Moreover, studies show that ketamine may activate the mTOR signaling pathway by p-mTOR induction to down-regulate the expression of crucial autophagic proteins such as LC3 and Beclin-1. According to these findings, ameliorating secondary brain injury and anti-inflammatory properties is closely related to the neuroprotection of ketamine, which supports the use of ketamine as a potential therapy for patients with TBI to alleviate functional deficits.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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