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Enriching neural stem cell and anti‐inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats
Author(s) -
Park Eunyoung,
Lyon Johnathan G.,
AlvaradoVelez Melissa,
Betancur Martha I.,
Mokarram Nassir,
Shin Jennifer H.,
Bellamkonda Ravi V.
Publication year - 2021
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.24834
Subject(s) - traumatic brain injury , microglia , neural stem cell , neuroinflammation , neuroregeneration , neuroscience , medicine , nestin , stimulation , stem cell , inflammation , central nervous system , immunology , psychology , biology , microbiology and biotechnology , psychiatry
Traumatic brain injury (TBI) by an external physical impact results in compromised brain function via undesired neuronal death. Following the injury, resident and peripheral immune cells, astrocytes, and neural stem cells (NSCs) cooperatively contribute to the recovery of the neuronal function after TBI. However, excessive pro‐inflammatory responses of immune cells, and the disappearance of endogenous NSCs at the injury site during the acute phase of TBI, can exacerbate TBI progression leading to incomplete healing. Therefore, positive outcomes may depend on early interventions to control the injury‐associated cellular milieu in the early phase of injury. Here, we explore electrical stimulation (ES) of the injury site in a rodent model (male Sprague–Dawley rats) to investigate its overall effect on the constituent brain cell phenotype and composition during the acute phase of TBI. Our data showed that a brief ES for 1 hr on day 2 of TBI promoted anti‐inflammatory phenotypes of microglia as assessed by CD206 expression and increased the population of NSCs and Nestin + astrocytes at 7 days post‐TBI. Also, ES effectively increased the number of viable neurons when compared to the unstimulated control group. Given the salience of microglia and neural stem cells for healing after TBI, our results strongly support the potential benefit of the therapeutic use of ES during the acute phase of TBI to regulate neuroinflammation and to enhance neuroregeneration.