A transgenic mouse model for inducible and reversible dysmyelination
Open accessAbstract
Oligodendrocytes are glial cells devoted to the production of myelin sheaths. Myelination of the CNS occurs essentially after birth. To delineate both the times of oligodendrocyte proliferation and myelination, as well as to study the consequence of dysmyelination in vivo, a model of inducible dysmyelination was developed. To achieve oligodendrocyte ablation, transgenic animals were generated that express the herpes virus 1 thymidine kinase (HSV1-TK) gene under the control of the myelin basic protein (MBP) gene promoter. The expression of the MBP-TK transgene in oligodendrocytes is not toxic on its own; however, toxicity can be selectively induced by the systemic injection of animals with nucleoside analogs, such as FIAU [1-(2-deoxy-2-fluoro-beta-delta-arabinofuranosyl)-5-iodouracil]. This system allows us to control the precise duration of the toxic insult and the degree of ablation of oligodendrocytes in vivo. We show that chronic treatment of MBP-TK mice with FIAU during the first 3 postnatal weeks triggers almost a total depletion of oligodendrocytes in the CNS. These effects are accompanied by a behavioral phenotype characterized by tremors, seizures, retarded growth, and premature animal death. We identify the period of highest oligodendrocytes division in the first 9 postnatal days. Delaying the beginning of FIAU treatments results in different degrees of dysmyelination. Dysmyelination in MBP-TK mice is always accompanied by astrocytosis. Thus, this transgenic line provides a model to study the events occurring during dysmyelination of various intensities. It also represents an invaluable tool to investigate remyelination in vivo.
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The Mbp promoter lacks the Schwann cell-specific enhancers required for activity in the peripheral nervous system.
“This would be an improvement over the Mbp promoter that lacks the Schwann cell-specific enhancers required for activity in the peripheral nervous system (Mathis et al., 2000).”
From Recombinant Human Myelin-Associated Glycoprotein Promoter Drives Selective AAV-Mediated Transgene Expression in Oligodendrocytes (2016) · cites this paper as Mathis et al., 2000
The Discussion says the MBP promoter fragment used in this model is not active in the PNS, and the CNS-restriction results report no sciatic-nerve dysmyelination. The paper does not establish that this fragment lacks Schwann cell-specific enhancers; it also notes that endogenous MBP transcripts are present in Schwann cells. The claim is therefore supported for the fragment’s PNS inactivity, but not for the stated enhancer explanation or for the MBP promoter generally. (LLM, conf=0.88)
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- Authors
- Mathis, C., Hindelang, C., LeMeur, M., & Borrelli, E.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2000-10-15
- Volume
- 20
- Issue
- 20
- Pages
- 7698-7705
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6772884
- OpenAlex
- W2122848200
- Cited by
- 42
- References
- 53
- Citations by year
- 2022: 1 · 2021: 1 · 2016: 2 · 2015: 1 · 2014: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Bristol-Myers Squibb
- Association pour la Recherche sur le Cancer
- Wellcome Trust
- Centre National de la Recherche Scientifique
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- dysmyelination, HSV-1 thymidine kinase, myelin basic protein promoter, FIAU, inducible gene expression, transgenic mouse model, oligodendrocyte proliferation, postnatal development, astrocyte activation, remyelination, seizures, tremor
- MeSH terms
- Animals, Antigens, Differentiation, Arabinofuranosyluracil, Brain, Demyelinating Diseases, Disease Models, Animal, Myelin Basic Protein, Female, Glial Fibrillary Acidic Protein, Gliosis, Male, Mice, Transgenic, Myelin Sheath, Oligodendroglia, Optic Nerve, Promoter Regions, Genetic, Recombinant Fusion Proteins, RNA, Messenger, Sciatic Nerve, Thymidine Kinase, Blotting, Northern, In Situ Hybridization, Herpesvirus 1, Human, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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