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Disruption and reorganization of sodium channels in experimental allergic neuritis
Author(s) -
Novakovic Sanja D.,
Levinson S. Rock,
Schachner Melitta,
Shrager Peter
Publication year - 1998
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199808)21:8<1019::aid-mus6>3.0.co;2-b
Subject(s) - node of ranvier , sodium channel , neuritis , electrophysiology , pathogenesis , neuroscience , ion channel , pathology , chemistry , medicine , myelin , anatomy , biology , central nervous system , sodium , receptor , organic chemistry
The axonal distribution of voltage‐dependent Na + channels was determined during inflammatory demyelinating disease of the peripheral nervous system. Experimental allergic neuritis was induced in Lewis rats by active immunization. In diseased spinal roots Na + channel immunofluorescence at many nodes of Ranvier changed from a highly focal ring to a more diffuse pattern and, as the disease progressed, eventually became undetectable. The loss of nodal channels corresponded closely with the development of clinical signs. Electrophysiological measurements and computations showed that a lateral spread of nodal Na + channels could contribute significantly to temperature sensitivity and conduction block. During recovery new clusters of Na + channels were seen. In fibers with large‐scale demyelination, the new aggregates formed at the edges of adhering Schwann cells and appeared to fuse to form new nodes. At nodes with demyelination limited to paranodal retraction, Na + channels were often found divided into two symmetric highly focal clusters. These results suggest that reorganization of Na + channels plays an important role in the pathogenesis of demyelinating neuropathies. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:1019–1032, 1998.