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Received: 13 June 2016 Revised: 29 December 2016 Accepted: 26 January 2017 DOI: 10.1002/brb3.667
ORIGINAL RESEARCH
Electrical stimulation improved cognitive deficits associated with traumatic brain injury in rats Zhi-tong Zheng1,2,3 | Xin-long Dong1,2,3 | Ya-dan Li4 | Wei-wei Gao1,2,3 | Yuan Zhou1,2,3 | Rong-cai Jiang1,2,3 | Shu-yuan Yue1 | Zi-wei Zhou1,2,3 | Jian-ning Zhang1,2,3 1 Department of Neurosurgery, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China 2
Key Laboratory of Post-trauma Neurorepair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China
3
Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China 4 Intensive Care Units, Tianjin Huanhu Hospital, Tianjin, China
Correspondence Zi-wei Zhou and Jian-ning Zhang, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China. Emails:
[email protected] and
[email protected] Funding information National Natural Science Foundation of China, Grant/Award Number: 81330029; Natural Science Foundations of Tianjin, Grant/Award Number: 13JCZDJC30800; Natural Science Foundations of Tianjin Medical University General Hospital, Grant/Award Number: 303071901401
Abstract Introduction: Cognitive deficits associated with traumatic brain injury (TBI) reduce patient quality of life. However, to date, there have been no effective treatments for TBI-associated cognitive deficits. In this study, we aimed to determine whether electrical stimulation (ES) improves cognitive deficits in TBI rats. Methods: Rats were randomly divided into three groups: the Sham control group, electrical stimulation group (ES group), and No electrical stimulation control group (N-ES group). Following fluid percussion injury, the rats in the ES group received ES treatment for 3 weeks. Potent cognitive function-relevant factors, including the escape latency, time percentage in the goal quadrant, and numbers of CD34+ cells, von Willebrand Factor+ (vWF+) vessels, and circulating endothelial progenitor cells (EPCs), were subsequently assessed using the Morris water maze (MWM) test, immunohistochemical staining, and flow cytometry. Results: Compared with the rats in the N-ES group, the rats in the ES group exhibited a shorter escape latency on day 3 (p = .025), day 4 (p = .011), and day 5 (p = .003), as well as a higher time percentage in the goal quadrant (p = .025) in the MWM test. After 3 weeks of ES, there were increased numbers of CD34+ cells (p = .008) and vWF+ vessels (p = .000) in the hippocampus of injured brain tissue in the ES group compared with those in the N-ES group. Moreover, ES also significantly increased the number of EPCs in the peripheral blood from days 3 to 21 after TBI in the ES group (p
