Riluzole protects against glutamate-induced slowing of neurofilament axonal transport

被引：27

作者：

Stevenson, Alison ^{[1
]}

Yates, Darran M. ^{[1
]}

Manser, Catherine ^{[1
]}

De Vos, Kurt J. ^{[1
]}

Vagnoni, Alessio ^{[1
]}

Leigh, P. Nigel ^{[1
]}

McLoughlin, Declan M. ^{[1
,2
,3
]}

Miller, Christopher C. J. ^{[1
]}

机构：

[1] Kings Coll London, Dept Neurosci P037, Inst Psychiat, MRC Ctr Neurodegenerat Res, London SE5 8AF, England

[2] St Patricks Hosp, Trinity Coll Dublin, Inst Neurosci, Dublin 8, Ireland

[3] St Patricks Hosp, Trinity Coll Dublin, Dept Psychiat, Dublin 8, Ireland

来源：

NEUROSCIENCE LETTERS | 2009年 / 454卷 / 02期

基金：

英国惠康基金;

关键词：

Amyotrophic lateral sclerosis; Motor neuron disease; Extracellular-regulated kinase; p38; Neurofilament; Axonal transport; AMYOTROPHIC-LATERAL-SCLEROSIS; LINKED SOD1 MUTANTS; PHOSPHATASE EXPRESSION; MOTOR-NEURONS; MOUSE MODEL; KINASE; DISEASE; ALS; PHOSPHORYLATION; INHIBITION;

D O I：

10.1016/j.neulet.2009.02.061

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：161 / 164

页数：4

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