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Reactive astrocytes prevent maladaptive plasticity after ischemic stroke

期刊

PROGRESS IN NEUROBIOLOGY
卷 209, 期 -, 页码 -

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2021.102199

关键词

Stroke; Recovery; Reactive gliosis; Intermediate filaments (nanofilaments); MRI; Functional connectivity

资金

  1. Friebe Foundation [T0498/28960/16]
  2. Swedish Medical Research Council [2017-02255, 2017-00991]
  3. ALF Gothenburg [724421, 716591]
  4. Sodderbergs' Foundations
  5. Hjadrnfonden
  6. Amlodv's Foundation
  7. Swedish Stroke Foundation
  8. EU FP 7 Program TargetBraIn [279017]
  9. Hagstrodmer's Foundation Millennium
  10. E. Jacobson's Donation Fund
  11. EuroCellNet COST Action [CA15214]
  12. Vinnova [2017-00991, 2017-02255] Funding Source: Vinnova
  13. Swedish Research Council [2017-00991, 2017-02255] Funding Source: Swedish Research Council

向作者/读者索取更多资源

The restoration of functional connectivity is crucial for functional recovery after stroke. This study investigated the role of reactive astrocytes in functional connectivity and recovery after ischemic stroke.
Restoration of functional connectivity is a major contributor to functional recovery after stroke. We investigated the role of reactive astrocytes in functional connectivity and recovery after photothrombotic stroke in mice with attenuated reactive gliosis (GFAP(-/-)Vim(-/-)). Infarct volume and longitudinal functional connectivity changes were determined by in vivo T2-weighted magnetic resonance imaging (MRI) and resting-state functional MRI. Sensorimotor function was assessed with behavioral tests, and glial and neural plasticity responses were quantified in the peri-infarct region. Four weeks after stroke, GFAP(-/-)Vim(-/-) mice showed impaired recovery of sensorimotor function and aberrant restoration of global neuronal connectivity. These mice also exhibited maladaptive plasticity responses, shown by higher number of lost and newly formed functional connections between primary and secondary targets of cortical stroke regions and increased peri-infarct expression of the axonal plasticity marker Gap43. We conclude that reactive astrocytes modulate recovery-promoting plasticity responses after ischemic stroke.

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