Enriching neural stem cell and anti-inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Park, E; Lyon, JG; Alvarado-Velez, M; Betancur, MI; Mokarram, N; Shin, JH; Bellamkonda, RV

Published Date

  • March 26, 2021

Published In

PubMed ID

  • 33772860

Pubmed Central ID

  • 33772860

Electronic International Standard Serial Number (EISSN)

  • 1097-4547

International Standard Serial Number (ISSN)

  • 0360-4012

Digital Object Identifier (DOI)

  • 10.1002/jnr.24834

Language

  • eng