This chapter discusses the role of various conduction blocking factors in multiple sclerosis and other inflammatory diseases. It is noted that conduction block which results from demyelination and axonal degeneration contribute to the production of clinical deficits in experimental models of demyelinating disease and in multiple sclerosis (MS), Guillain-Barré syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy. A variety of putative blocking factors have been proposed over the last four decades including antibodies, cytokines, small peptides, and nitric oxide. Many of these blocking factors that have been investigated are thought to target voltage-gated sodium channels. Several mechanisms by which drugs and other factors can reduce the activity of voltage-gated sodium channels have been identified. Some biological toxins, such as tetrodotoxin, directly block sodium currents by binding in the pore of the channel and preventing the flow of sodium ions through the pore. Furthermore, modulation of other channels or membrane proteins might also contribute to block of impulse transmission, most of the work on the role of blocking factors in inflammatory demyelinating diseases has focused on voltage-gated sodium channels.
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