Disruption and reorganization of sodium channels in experimental allergic neuritis
- PMID: 9655120
- DOI: 10.1002/(sici)1097-4598(199808)21:8<1019::aid-mus6>3.0.co;2-b
Disruption and reorganization of sodium channels in experimental allergic neuritis
Abstract
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.
Similar articles
-
Disruption of neurofascin and gliomedin at nodes of Ranvier precedes demyelination in experimental allergic neuritis.Brain. 2009 Jan;132(Pt 1):260-73. doi: 10.1093/brain/awn281. Epub 2008 Oct 25. Brain. 2009. PMID: 18953054
-
Changes of ionic channel distribution in myelinated nerve fibres from rats with experimental allergic neuritis.Neurosci Lett. 1991 Jan 28;122(2):205-9. doi: 10.1016/0304-3940(91)90859-r. Neurosci Lett. 1991. PMID: 1709262
-
Simulating perinodal changes observed in immune-mediated neuropathies: impact on conduction in a model of myelinated motor and sensory axons.J Neurophysiol. 2019 Sep 1;122(3):1036-1049. doi: 10.1152/jn.00326.2019. Epub 2019 Jul 10. J Neurophysiol. 2019. PMID: 31291151
-
Conduction block in demyelinated axons precipitated by normally innocuous physiological processes.Suppl Clin Neurophysiol. 2004;57:191-4. doi: 10.1016/s1567-424x(09)70357-5. Suppl Clin Neurophysiol. 2004. PMID: 16106619 Review. No abstract available.
-
The local differentiation of myelinated axons at nodes of Ranvier.Nat Rev Neurosci. 2003 Dec;4(12):968-80. doi: 10.1038/nrn1253. Nat Rev Neurosci. 2003. PMID: 14682359 Review.
Cited by
-
Electrophysiology of Guillain-Barré syndrome in Bangladesh: A prospective study of 312 patients.Clin Neurophysiol Pract. 2021 Apr 22;6:155-163. doi: 10.1016/j.cnp.2021.03.007. eCollection 2021. Clin Neurophysiol Pract. 2021. PMID: 35112034 Free PMC article.
-
Nav1.6 promotes inflammation and neuronal degeneration in a mouse model of multiple sclerosis.J Neuroinflammation. 2019 Nov 13;16(1):215. doi: 10.1186/s12974-019-1622-1. J Neuroinflammation. 2019. PMID: 31722722 Free PMC article.
-
Immunostaining in whole-mount lipid-cleared peripheral nerves and dorsal root ganglia after neuropathy in mice.Sci Rep. 2019 Jun 10;9(1):8374. doi: 10.1038/s41598-019-44897-7. Sci Rep. 2019. PMID: 31182787 Free PMC article.
-
The evolution of vertebrate and invertebrate myelin: a theoretical computational study.J Comput Neurosci. 2015 Jun;38(3):521-38. doi: 10.1007/s10827-015-0552-x. Epub 2015 Apr 2. J Comput Neurosci. 2015. PMID: 25832903
-
Animal models of autoimmune neuropathy.ILAR J. 2014;54(3):282-90. doi: 10.1093/ilar/ilt054. ILAR J. 2014. PMID: 24615441 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
