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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
Published on: March 26, 2015
Spinal cord dysmyelination induced in vivo by IgM antibodies to three different myelin glycolipids
J Rosenbluth1, W L Liang, R Schiff
1Department of Physiology and Neuroscience, Rusk Institute of Rehabilitation Medicine, New York University School of Medicine, New York 10016, USA.
It was shown previously (Rosenbluth et al.: J. Neurosci. 16:2635-2641, 1996) that implantation of hybridoma cells that produce an IgM antigalactocerebroside into the spinal cord of young rats results in the development of myelin sheaths with a repeat period approximately 2-3x normal, similar to the abnormal peripheral myelin sheaths seen in human IgM gammopathies. We now present evidence that this effect can be reproduced in the spinal cord by implanting either of two other hybridomas, O4 and A2B5, that secrete, respectively, antisulfatide and antiganglioside IgM antibodies. The formation of expanded CNS myelin thus does not depend on antibodies to galactocerebroside specifically but can be mediated by IgM antibodies that react with other myelin glycolipids as well.
It was shown previously (Rosenbluth et al.: J. Neurosci. 16:2635-2641, 1996) that implantation of hybridoma cells that produce an IgM antigalactocerebroside into the spinal cord of young rats results in the development of myelin sheaths with a repeat period approximately 2-3x normal, similar to the abnormal peripheral myelin sheaths seen in human IgM gammopathies. We now present evidence that this effect can be reproduced in the spinal cord by implanting either of two other hybridomas, O4 and A2B5, that secrete, respectively, antisulfatide and antiganglioside IgM antibodies. The formation of expanded CNS myelin thus does not depend on antibodies to galactocerebroside specifically but can be mediated by IgM antibodies that react with other myelin glycolipids as well.
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