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Brain Advance Access published online on June 9, 2006
Brain, doi:10.1093/brain/awl144
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received February 3, 2006
Revised April 9, 2006
Accepted May 5, 2006

Article

Nodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosis

I. Coman 1, M. S. Aigrot 2, D. Seilhean 3, R. Reynolds 4, J. A. Girault 5, B. Zalc 2, and C. Lubetzki 1 *

1 INSERM U711, Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France; Université Pierre & Marie Curie (UPMC Paris 6), Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France; AP-HP, Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France
2 INSERM U711, Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France; Université Pierre & Marie Curie (UPMC Paris 6), Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France
3 Laboratoire de Neuropathologie IFR-70, Paris, France
4 Department of Cellular and Molecular Neuroscience, Imperial College London, London, UK
5 Université Pierre & Marie Curie (UPMC Paris 6), Hôpital de la Salpêtrière, Fédération des maladies du système nerveux, Paris, France; INSERM U536, Paris, France

* To whom correspondence should be addressed.
C. Lubetzki, E-mail: catherine.lubetzki{at}psl.ap-hop-paris.fr


  Abstract

Saltatory conduction in myelinated fibres depends on the specific molecular organization of highly specialized axonal domains at the node of Ranvier, the paranodal and the juxtaparanodal regions. Voltage-gated sodium channels (Nav) have been shown to be deployed along the naked demyelinated axon in experimental models of CNS demyelination and in multiple sclerosis lesions. Little is known about aggregation of nodal, paranodal and juxtaparanodal constituents during the repair process. We analysed by immunohistochemistry on free-floating sections from multiple sclerosis brains the expression and distribution of nodal (Nav channels), paranodal (paranodin/Caspr) and juxtaparanodal (Kv channels and Caspr2) molecules in demyelinated and remyelinated lesions. Whereas in demyelinated lesions, paranodal and juxtaparanodal proteins are diffusely distributed on denuded axons, the distribution of Nav channels is heterogeneous, with a diffuse immunoreactivity but also few broad Nav channel aggregates in all demyelinated lesions. In contrast to the demyelinated plaques, all remyelinated lesions are characterized by the detection of aggregates of Nav channels, paranodin/Caspr, Kv channels and Caspr2. Our data suggest that these aggregates precede remyelination, and that Nav channel aggregation is the initial event, followed by aggregation of paranodal and then juxtaparanodal axonal proteins. Remyelination takes place in multiple sclerosis tissue but myelin repair is often incomplete, and the reasons for this remyelination deficit are many. We suggest that a defect of Nav channel aggregation might be involved in the remyelination failure in demyelinated lesions with spared axons and oligodendroglial cells.

Keywords: multiple sclerosis; demyelination; remyelination; sodium channels; potassium channels.
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