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. 2017 Oct 5;7(11):e00667.
doi: 10.1002/brb3.667. eCollection 2017 Nov.

Electrical stimulation improved cognitive deficits associated with traumatic brain injury in rats

Zhi-Tong Zheng  1   2   3 , Xin-Long Dong  1   2   3 , Ya-Dan Li  4 , Wei-Wei Gao  1   2   3 , Yuan Zhou  1   2   3 , Rong-Cai Jiang  1   2   3 , Shu-Yuan Yue  1 , Zi-Wei Zhou  1   2   3 , Jian-Ning Zhang  1   2   3
Affiliations

Electrical stimulation improved cognitive deficits associated with traumatic brain injury in rats

Zhi-Tong Zheng et al. Brain Behav. .

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 < .05).

Conclusions: Taken together, these findings suggest that ES may improve cognitive deficits induced by TBI, and this protective effect may be a result, in part, of enhanced angiogenesis, which may be attributed to the increased mobilization of EPCs in peripheral blood.

Keywords: angiogenesis; cognitive deficit; electrical stimulation; endothelial progenitor cell; traumatic brain injury.

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Figures

Figure 1
Figure 1
Electrical stimulation (ES) treatment significantly improved the cognitive deficit associated with traumatic brain injury (TBI) by Morris water maze tests. (a) This data suggested that the escape latency of all rats was influenced by grouping. The test revealed that the escape latency in Sham group was significantly shorter than that in the N‐ES group from day 2 to 5. And there was no difference between Sham group and ES group. Furthermore, the escape latency was significantly decreased in ES group compared to N‐ES group from day 3 to 5. (b) Six days after training, the platform was removed and the ability of rats to find the removed platform through spatial memory was measured as percent of times they swam in the goal quadrant. Compared with the N‐ES group, rats in the ES group had significantly increased time percents in goal quadrant. However, there was no difference to the percents between ES group and Sham group. n = 10/group; *p < .05 ES group versus N‐ES group; # p < .05 N‐ES group and ES group versus Sham group
Figure 2
Figure 2
Detection of CD34+ cells in the CA1 region, a subdivision of Ammon's horn of hippocampus, of the injured side after electrical stimulation treatment by immunohistochemistry staining. (a) Sham group, (b) no electrical stimulation(N‐ES) group, (c) electrical stimulation (ES) group, (d) quantitative data of CD34 positive cells. The classical CD34+ cells are directed by black arrow. They were defined as the cells which are spindle‐shape and brown staining. n = 6/group; *p < .05 ES group versus N‐ES group; # p < .05 N‐ES group and ES group versus Sham group
Figure 3
Figure 3
Detection of von Willebrand Factor (VWF)+ vessels in the CA1 region, a subdivision of Ammon's horn of hippocampus, of the injured side after electrical stimulation treatment by immunohistochemistry staining. (a) Sham group, (b) NES group, (c) ES group, (d) quantitative data of VWF positive vessels. The classical VWF + vessels are directed by black arrow, and which have the brown staining lumina formation. n = 6/group; *p < .05 ES group versus NES group; # p < .05 N‐ES group and ES group versus Sham group
Figure 4
Figure 4
Flow cytometry detection of endothelial progenitor cells (EPCs) in peripheral blood of rats before the traumatic brain injury (TBI) (0 day), and 1, 3, 7, 14, 21, 28 days after TBI. They were marked by CD34 and CD133. The stress of TBI mobilized the EPCs at 1 day after TBI in N‐ES group and ES group. Electrical stimulation treatment increased EPCs numbers in peripheral blood from 3 to 21 days after TBI. n = 6/group; *p < .05 ES group versus N‐ES group; # p < .05 N‐ES group and ES group versus Sham group
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