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Research Article| Volume 64, ISSUE 3, P297-303, June 1984

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Antigalactocerebroside serum demyelinates optic nerve in vivo

  • Robert C. Sergott
    Correspondence
    Address reprint requests to Robert C. Sergott, M.D., Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, U.S.A.
    Affiliations
    Department of Neurology, University of Pennsylvania School of Medicine Philadelphia, PA 19104 U.S.A.

    Department of Ophthalmology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 U.S.A.
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  • Mark J. Brown
    Affiliations
    Department of Neurology, University of Pennsylvania School of Medicine Philadelphia, PA 19104 U.S.A.

    Department of Ophthalmology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 U.S.A.
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  • Donald H. Silberberg
    Affiliations
    Department of Neurology, University of Pennsylvania School of Medicine Philadelphia, PA 19104 U.S.A.

    Department of Ophthalmology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 U.S.A.
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  • Robert P. Lisak
    Affiliations
    Department of Neurology, University of Pennsylvania School of Medicine Philadelphia, PA 19104 U.S.A.

    Department of Ophthalmology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 U.S.A.
    Search for articles by this author
DOI:https://doi.org/10.1016/0022-510X(84)90177-1
Antigalactocerebroside serum demyelinates optic nerve in vivo
Previous ArticleCorrelated nerve conduction, somatosensory evoked potential and neuropathological studies in clioquinol and 2,5-hexanedione neurotoxicity in the baboon
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      Abstract

      Antiserum to the myelin lipid galactocerebroside (GalC) causes rapidly progressive focal demyelination when injected into guinea pig optic nerves. The capacity of anti-GalC to induce central nervous system demyelination is complement-dependent, and demyelinating activity is present in the immunoglobulin fraction of anti-GalC serum. Demyelination appears to result from primary damage to oligodendrocytes.

      Keywords

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      Article info

      Publication history

      Accepted: February 7, 1984
      Received in revised form: February 7, 1984
      Received: August 29, 1983

      Footnotes

      ☆This project was supported by grants from the NIH (NS-11037, NS-08075), the Kroc Foundation, the National Multiple Sclerosis Society, and a research fellowship grant from the Heed Ophthalmic Foundation.

      Identification

      DOI: https://doi.org/10.1016/0022-510X(84)90177-1

      Copyright

      © 1984 Published by Elsevier Inc.

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