Source:http://linkedlifedata.com/resource/pubmed/id/17219031
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2007-1-12
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pubmed:abstractText |
Axonal degeneration is a major cause of permanent disability in multiple sclerosis (MS). Recent observations from our and other laboratories suggest that sodium accumulation within compromised axons is a key, early step in the degenerative process, and hence that limiting axonal sodium influx may represent a mechanism for axonal protection in MS. Here we assess whether lamotrigine, a sodium channel-blocking agent, is effective in preventing axonal degeneration in an animal model of MS, namely chronic-relapsing experimental autoimmune encephalomyelitis (CR-EAE). When administered from 7 days post-inoculation, lamotrigine provided a small but significant reduction in the neurological deficit present at the termination of the experiments (averaged over three independent experiments; vehicle: 3.5+/-2.7; lamotrigine: 2.6+/-2.0, P<0.05) and preserved more functional axons in the spinal cord (measured as mean compound action potential area; vehicle: 31.7 microV.ms+/-23.0; lamotrigine: 42.9+/-27.4, P<0.05). Histological examination of the thoracic spinal cord (n=71) revealed that lamotrigine treatment also provided significant protection against axonal degeneration (percentage degeneration in dorsal column; vehicle: 33.5 %+/-38.5; lamotrigine: 10.4 %+/-12.5, P<0.01). The findings suggest that lamotrigine may provide a novel avenue for axonal protection in MS.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0340-5354
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
253
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1542-51
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pubmed:dateRevised |
2011-11-3
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pubmed:meshHeading |
pubmed-meshheading:17219031-Action Potentials,
pubmed-meshheading:17219031-Animals,
pubmed-meshheading:17219031-Disease Models, Animal,
pubmed-meshheading:17219031-Dose-Response Relationship, Drug,
pubmed-meshheading:17219031-Male,
pubmed-meshheading:17219031-Multiple Sclerosis,
pubmed-meshheading:17219031-Nerve Degeneration,
pubmed-meshheading:17219031-Neuroprotective Agents,
pubmed-meshheading:17219031-Rats,
pubmed-meshheading:17219031-Spinal Cord,
pubmed-meshheading:17219031-Statistics, Nonparametric,
pubmed-meshheading:17219031-Time Factors,
pubmed-meshheading:17219031-Triazines
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pubmed:year |
2006
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pubmed:articleTitle |
Axonal protection achieved in a model of multiple sclerosis using lamotrigine.
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pubmed:affiliation |
Department of Clinical Neuroscience, King's College London, Guy's Campus, National Hospital for Neurology and Neurosurgery, London, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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