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dc.contributor.authorStevenson, Alison
dc.contributor.authorYates, Darran M
dc.contributor.authorManser, Catherine
dc.contributor.authorDe Vos, Kurt J
dc.contributor.authorVagnoni, Alessio
dc.contributor.authorLeigh, P Nigel
dc.contributor.authorMcLoughlin, Declan M
dc.contributor.authorMiller, Christopher C J
dc.date.accessioned2011-04-27T09:27:26Z
dc.date.available2011-04-27T09:27:26Z
dc.date.issued2009-04-24
dc.identifier.citationRiluzole protects against glutamate-induced slowing of neurofilament axonal transport. 2009, 454 (2):161-4 Neurosci. Lett.en
dc.identifier.issn0304-3940
dc.identifier.pmid19429076
dc.identifier.doi10.1016/j.neulet.2009.02.061
dc.identifier.urihttp://hdl.handle.net/10147/128718
dc.description.abstractRiluzole 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.
dc.language.isoenen
dc.relation.urldoi:10.1016/j.neulet.2009.02.061en
dc.subject.meshAnalysis of Variance
dc.subject.meshAnimals
dc.subject.meshAxonal Transport
dc.subject.meshAxons
dc.subject.meshBrain
dc.subject.meshCells, Cultured
dc.subject.meshDose-Response Relationship, Drug
dc.subject.meshExcitatory Amino Acid Antagonists
dc.subject.meshExtracellular Signal-Regulated MAP Kinases
dc.subject.meshGlutamic Acid
dc.subject.meshImmunohistochemistry
dc.subject.meshNeurofilament Proteins
dc.subject.meshNeurons
dc.subject.meshNeuroprotective Agents
dc.subject.meshPhosphorylation
dc.subject.meshRats
dc.subject.meshRiluzole
dc.subject.meshp38 Mitogen-Activated Protein Kinases
dc.titleRiluzole protects against glutamate-induced slowing of neurofilament axonal transport.en
dc.typeArticleen
dc.contributor.departmentMRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College, London, UK.en
dc.identifier.journalNeuroscience lettersen
dc.description.provinceLeinster
html.description.abstractRiluzole 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.


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