Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination - PubMed (original) (raw)
doi: 10.1038/ng1095. Epub 2003 Feb 18.
Affiliations
- PMID: 12590258
- DOI: 10.1038/ng1095
Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination
Corinna Lappe-Siefke et al. Nat Genet. 2003 Mar.
Abstract
Myelination of axons by oligodendrocytes enables rapid impulse propagation in the central nervous system. But long-term interactions between axons and their myelin sheaths are poorly understood. Here we show that Cnp1, which encodes 2',3'-cyclic nucleotide phosphodiesterase in oligodendrocytes, is essential for axonal survival but not for myelin assembly. In the absence of glial cyclic nucleotide phosphodiesterase, mice developed axonal swellings and neurodegeneration throughout the brain, leading to hydrocephalus and premature death. But, in contrast to previously studied myelin mutants, the ultrastructure, periodicity and physical stability of myelin were not altered in these mice. Genetically, the chief function of glia in supporting axonal integrity can thus be completely uncoupled from its function in maintaining compact myelin. Oligodendrocyte dysfunction, such as that in multiple sclerosis lesions, may suffice to cause secondary axonal loss.
Comment in
- Myelin: not just a conduit for conduction.
Popko B. Popko B. Nat Genet. 2003 Mar;33(3):327-8. doi: 10.1038/ng0303-327. Nat Genet. 2003. PMID: 12610543 No abstract available.
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