ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Recovery of myelin after induction of oligodendrocyte cell death in postnatal brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Intranasal stem cell treatment ameliorates neuroinflammation and myelin aberrations in fetal growth-restricted rat pups.Stem cells translational medicine · 2026Article
- White-Matter Repair as a Novel Therapeutic Target for Early Adversity.Frontiers in neuroscience · 2021Review
- Histone acetylation as a new mechanism for bilirubin-induced encephalopathy in the Gunn rat.Scientific reports · 2018Article
- B-1a lymphocytes promote oligodendrogenesis during brain development.Nature neuroscience · 2018Article
- Embracing oligodendrocyte diversity in the context of perinatal injury.Neural regeneration research · 2017Review
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- The neural androgen receptor: a therapeutic target for myelin repair in chronic demyelination.Brain : a journal of neurology · 2013Article
- Article
- Reactive astrocytes form scar-like perivascular barriers to leukocytes during adaptive immune inflammation of the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Recovery from chronic demyelination by thyroid hormone therapy: myelinogenesis induction and assessment by diffusion tensor magnetic resonance imaging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Systemic prenatal insults disrupt telencephalon development: implications for potential interventions.Epilepsy & behavior : E&B · 2005Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A transgenic mouse line (Oligo-TTK) was established to monitor oligodendrocyte cell death and myelin formation in the CNS. The expression of a conditionally toxic gene, the herpes simplex virus-1 thymidine kinase (HSV1-TK), was made under control of the MBP (myelin basic protein) gene promoter. A truncated form of the HSV1-TK (TTK) gene was used to avoid both bystander effect resulting from leaking in thymidine kinase activity and sterility in transgenic males observed in previous transgenic mice. The transgene was expressed in the CNS with a restricted localization in oligodendrocytes. Oligodendrocyte proliferation and myelin formation are therefore tightly controlled experimentally by administration of ganciclovir (GCV) via the induction of oligodendrocyte cell death. The most severe and irreversible hypomyelination was obtained when GCV was given daily from postnatal day 1 (P1) to P30. Oligodendrocyte plasticity and myelin recovery were analyzed in another phenotype generated by GCV treatment from P1 to P15. In this model, after dysmyelination, an apparent normal behavior was restored with no visible pathological symptoms by P30. Proliferating cells, which may be implicated in myelin repair in this model, are detected primarily in myelin tracts expressing the oligodendrocyte phenotype. Therefore, the endogenous potential of oligodendrocytes to remyelinate was clearly demonstrated in the mice of this study.
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