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

Abstract

IntroductionCognitive 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.MethodsRats 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.ResultsCompared 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).ConclusionsTaken 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.

Excitation of the Pre-frontal and Primary Visual Cortex in Response to Transcorneal Electrical Stimulation in Retinal Degeneration Mice

“…We employed the use of sham rd10 controls in our experimental design because we wanted to evaluate the effect of our TES procedure in an unbiased fashion by ensuring that the observed modulatory effects are due to the applied electrical stimulation instead of being caused by other ancillary factors. Sham controls are documented to be widely used in basic and clinical research ( Naycheva et al, 2013 ; Bola et al, 2014 ; Zheng et al, 2017 ). Moreover, a good number of studies in retinal electrical stimulation genre including preclinical studies on rodents and clinical studies have also employed the use of sham controls ( Henrich-Noack et al, 2013 ; Sehic et al, 2016 ; Bittner et al, 2017 ; Schatz et al, 2017 ).…”

Towards Novel Geneless Approaches for Therapeutic Angiogenesis

“…Moreover, electrical stimulation promoted the formation of capillaries and arterioles in a mouse model of ischemia, while attenuating muscle necrosis and fibrosis and eventually preventing loss of the injured limb. Interestingly, it was also reported that electrical stimulation significantly increases, among other effects, the number of EPCs in the peripheral blood of rats subjected to fluid percussion injury ( Zheng et al, 2017 ). Magnetic field-guided transplantation of silica-coated magnetic iron oxide nanoparticle-labeled EPCs was associated with their enhanced aggregation in the infarcted border zone ( Zhang et al, 2019 ).…”

Novel Electrode Designs for Neurostimulation in Regenerative Medicine: Activation of Stem Cells

“…Notably, electrical stimulation can elicit other cellular responses, such as cell proliferation. 19 Interestingly, electrical stimulation has been shown to increase the number of blood vessels in the injured brain, 42 modulate blood-brain barrier permeability, 43,44 and modulate numbers of microglia and astrocytes. [45][46][47][48] The ability to affect the microenvironment creates the possibility of ''side effects'' such as modulation of the number of astrocytes and microglia but with more insight into the effects of EFs on tissue responses; these ''side effects'' could be purposely controlled to create an environment more amenable to tissue repair.…”