Here's a fairly recent article (from Yale University, so I believe it could be thought of as highly credible) that again connects maintaining sodium density with preventing axonal degeneration (axonal degeneration has been found to be what produces permanent disability in MS). I have posted other findings and postulated on regulation of ion sodium channel density in previous threads and discussions. I touched upon the role of Na(v) before, also.
The mention within this article of tetrodotoxin (which is a highly toxic substance found in puffer fish), is not indicative of a direct treatment for MS, though. I quote from http://www.chm.bris.ac.uk/motm/ttx/ttx.htm:
Quote:
A single milligram or less of TTX - an amount that can be placed on the head of a pin, is enough to kill an adult.
Its use in this research was simply as an agent for producing desired results as it pertained to sodium density, but not as a treatment source.
Anyway, there is other research going on regarding treatment agents to help maintain sodium density, but I won't go into those links right now.
I thought this might be an interesting article for some folks here, as we have recently shared theories regarding ion channels, sodium density, and axonal degeneration in MS.
I'd like to point out again, how important the migration of microglia and macrophages in MS appears to be, and how inhibiting that activation appears to be highly beneficial.
Deb
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Glia. 2005 Jan 15;49(2):220-9. Related Articles, Links
Sodium channels contribute to microglia/macrophage activation and function in EAE and MS.
Craner MJ, Damarjian TG, Liu S, Hains BC, Lo AC, Black JA, Newcombe J, Cuzner ML, Waxman SG.
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut.
Loss of axons is a major contributor to nonremitting deficits in the inflammatory demyelinating disease multiple sclerosis (MS). Based on biophysical studies showing that activity of axonal sodium channels can trigger axonal degeneration, recent studies have tested sodium channel-blocking drugs in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and have demonstrated a protective effect on axons. However, it is possible that, in addition to a direct effect on axons, sodium channel blockers may also interfere with inflammatory mechanisms. We therefore examined the novel hypothesis that sodium channels contribute to activation of microglia and macrophages in EAE and acute MS lesions. In this study, we demonstrate a robust increase of sodium channel Na(v)1.6 expression in activated microglia and macrophages in EAE and MS. We further demonstrate that treatment with the sodium channel blocker phenytoin ameliorates the inflammatory cell infiltrate in EAE by 75%. Supporting a role for sodium channels in microglial activation, we show that tetrodotoxin, a specific sodium channel blocker, reduces the phagocytic function of activated rat microglia by 40%. To further confirm a role of Na(v)1.6 in microglial activation, we examined the phagocytic capacity of microglia from med mice, which lack Na(v)1.6 channels, and show a 65% reduction in phagocytic capacity compared with microglia from wildtype mice. Our findings indicate that sodium channels are important for activation and phagocytosis of microglia and macrophages in EAE and MS and suggest that, in addition to a direct neuroprotective effect on axons, sodium channel blockade may ameliorate neuroinflammatory disorders via anti-inflammatory mechanisms. (c) 2004 Wiley-Liss, Inc.
PMID: 15390090 [PubMed - in process]
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(I thought you were taking a nap, Robin.)
