Abstract
leakage of sodium current in the demyelinated region. We propose voltage-gated sodium channel (VGSC) gating modifiers as a novel strategy for multiple sclerosis symptom treatment. Since different VGSC toxins are available, we can change the VGSC function in an arbitrary way. Some well-recognized VGSC modifiers can shift the voltage dependence of the activation gate to more hyperpolarized potentials and inhibit the channel inactivation gate. On the other hand, some VGSCs stabilize the open state of the channel. For example, Alpha-scorpion toxin, sea anemone toxins, and some spider toxins postpone sodium channel inactivation. Experimental data show that the effect of these toxins facilitates the stimulation of VGSC and can increase the flow of
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