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Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion.

Publication ,  Journal Article
Noebels, JL; Marcom, PK; Jalilian-Tehrani, MH
Published in: Nature
August 1, 1991

Trophic control over the expression and membrane distribution of voltage-dependent ion channels is one of the principal organizing events underlying the maturation of excitable cells. The myelin sheath is a major structural determinant of regional ion channel topography in central axons, but the exact molecular signals that mediate local interactions between the oligodendrocyte and axolemma are not known. We have found that large caliber fibre pathways in the brain of the mutant mouse shiverer (shi, gene on chromosome 18), whose developmental fate of myelination is averted by deletion of five exons in the myelin basic protein gene, have a striking excess of sodium channels. As cytoplasmic membranes of shiverer oligodendroglia still adhere to axons, the evidence indicates that myelin basic protein or a myelin basic protein-dependent glial transmembrane signal associated with compact myelin formation, rather than a simple glial-axon contact inhibition or an intrinsic genetic program of neuronal differentiation, could be critical in downregulating sodium channel density in axons. Here we use the shiverer mutant to show that mature central nervous system projection neurons with large caliber unmyelinated fibres sustain functional excitability by increasing sodium channel density. This axon plasticity, triggered by the absence of a single glial protein, contributes to the unexpectedly mild degree of neurological impairment in the mutant brain without myelin, and may be a potentially inducible mechanism determining the recovery of function from dysmyelinating disease.

Duke Scholars

Published In

Nature

DOI

ISSN

0028-0836

Publication Date

August 1, 1991

Volume

352

Issue

6334

Start / End Page

431 / 434

Location

England

Related Subject Headings

  • Sodium Channels
  • Saxitoxin
  • Oligodendroglia
  • Nerve Fibers
  • Myelin Sheath
  • Myelin Basic Protein
  • Mice, Neurologic Mutants
  • Mice
  • General Science & Technology
  • Exons
 

Citation

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Noebels, J. L., Marcom, P. K., & Jalilian-Tehrani, M. H. (1991). Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion. Nature, 352(6334), 431–434. https://doi.org/10.1038/352431a0
Noebels, J. L., P. K. Marcom, and M. H. Jalilian-Tehrani. “Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion.Nature 352, no. 6334 (August 1, 1991): 431–34. https://doi.org/10.1038/352431a0.
Noebels JL, Marcom PK, Jalilian-Tehrani MH. Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion. Nature. 1991 Aug 1;352(6334):431–4.
Noebels, J. L., et al. “Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion.Nature, vol. 352, no. 6334, Aug. 1991, pp. 431–34. Pubmed, doi:10.1038/352431a0.
Noebels JL, Marcom PK, Jalilian-Tehrani MH. Sodium channel density in hypomyelinated brain increased by myelin basic protein gene deletion. Nature. 1991 Aug 1;352(6334):431–434.
Journal cover image

Published In

Nature

DOI

ISSN

0028-0836

Publication Date

August 1, 1991

Volume

352

Issue

6334

Start / End Page

431 / 434

Location

England

Related Subject Headings

  • Sodium Channels
  • Saxitoxin
  • Oligodendroglia
  • Nerve Fibers
  • Myelin Sheath
  • Myelin Basic Protein
  • Mice, Neurologic Mutants
  • Mice
  • General Science & Technology
  • Exons