Environmental enrichment ameliorates perinatal brain injury and promotes functional white matter recovery.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
19 02 2020
Historique:
received: 17 04 2018
accepted: 31 01 2020
entrez: 21 2 2020
pubmed: 23 2 2020
medline: 30 4 2020
Statut: epublish

Résumé

Hypoxic damage to the developing brain due to preterm birth causes many anatomical changes, including damage to the periventricular white matter. This results in the loss of glial cells, significant disruptions in myelination, and thereby cognitive and behavioral disabilities seen throughout life. Encouragingly, these neurological morbidities can be improved by environmental factors; however, the underlying cellular mechanisms remain unknown. We found that early and continuous environmental enrichment selectively enhances endogenous repair of the developing white matter by promoting oligodendroglial maturation, myelination, and functional recovery after perinatal brain injury. These effects require increased exposure to socialization, physical activity, and cognitive enhancement of surroundings-a complete enriched environment. Using RNA-sequencing, we identified oligodendroglial-specific responses to hypoxic brain injury, and uncovered molecular mechanisms involved in enrichment-induced recovery. Together, these results indicate that myelin plasticity induced by modulation of the neonatal environment can be targeted as a therapeutic strategy for preterm birth.

Identifiants

pubmed: 32075970
doi: 10.1038/s41467-020-14762-7
pii: 10.1038/s41467-020-14762-7
pmc: PMC7031237
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

964

Subventions

Organisme : NINDS NIH HHS
ID : F31 NS100277
Pays : United States
Organisme : NICHD NIH HHS
ID : U54 HD090257
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR001877
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001876
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS099461
Pays : United States
Organisme : NINDS NIH HHS
ID : F32 NS106723
Pays : United States
Organisme : NINDS NIH HHS
ID : R37 NS109478
Pays : United States

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Auteurs

Thomas A Forbes (TA)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.
Institute for Biomedical Sciences, The George Washington University, Washington, DC, 20052, USA.

Evan Z Goldstein (EZ)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.

Jeffrey L Dupree (JL)

Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA, 23284, USA.

Beata Jablonska (B)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.
Institute for Biomedical Sciences, The George Washington University, Washington, DC, 20052, USA.

Joseph Scafidi (J)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.
Institute for Biomedical Sciences, The George Washington University, Washington, DC, 20052, USA.

Katrina L Adams (KL)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.

Yuka Imamura (Y)

Institute for Personalized Medicine, Penn State University, College of Medicine, Hershey, PA, 17033, USA.

Kazue Hashimoto-Torii (K)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA.

Vittorio Gallo (V)

Center for Neuroscience Research, Children's Research Institute, Children's National Hospital, Washington, DC, 20010, USA. vgallo@cnmcresearch.org.
Institute for Biomedical Sciences, The George Washington University, Washington, DC, 20052, USA. vgallo@cnmcresearch.org.

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