Riluzole protects against glutamate-induced slowing of neurofilament axonal transport.
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Authors
Stevenson, AlisonYates, Darran M
Manser, Catherine
De Vos, Kurt J
Vagnoni, Alessio
Leigh, P Nigel
McLoughlin, Declan M
Miller, Christopher C J
Affiliation
MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College, London, UK.Issue Date
2009-04-24MeSH
Analysis of VarianceAnimals
Axonal Transport
Axons
Brain
Cells, Cultured
Dose-Response Relationship, Drug
Excitatory Amino Acid Antagonists
Extracellular Signal-Regulated MAP Kinases
Glutamic Acid
Immunohistochemistry
Neurofilament Proteins
Neurons
Neuroprotective Agents
Phosphorylation
Rats
Riluzole
p38 Mitogen-Activated Protein Kinases
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Riluzole protects against glutamate-induced slowing of neurofilament axonal transport. 2009, 454 (2):161-4 Neurosci. Lett.Journal
Neuroscience lettersDOI
10.1016/j.neulet.2009.02.061PubMed ID
19429076Additional Links
doi:10.1016/j.neulet.2009.02.061Abstract
Riluzole is the only drug approved for the treatment of amyotrophic lateral sclerosis (ALS) but its precise mode of action is not properly understood. Damage to axonal transport of neurofilaments is believed to be part of the pathogenic mechanism in ALS and this has been linked to defective glutamate handling and increased phosphorylation of neurofilament side-arm domains. Here, we show that riluzole protects against glutamate-induced slowing of neurofilament transport. Protection is associated with decreased neurofilament side-arm phosphorylation and inhibition of the activities of two neurofilament kinases, ERK and p38 that are activated in ALS. Thus, the anti-glutamatergic properties of riluzole include protection against glutamate-induced changes to neurofilament phosphorylation and transport.Item Type
ArticleLanguage
enISSN
0304-3940ae974a485f413a2113503eed53cd6c53
10.1016/j.neulet.2009.02.061
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