Show simple item record

dc.contributor.authorCarbone, M.
dc.contributor.authorDuty, S.
dc.contributor.authorRattray, Marcus
dc.date.accessioned2016-02-23T16:28:40Z
dc.date.available2016-02-23T16:28:40Z
dc.date.issued2012-04
dc.identifier.citationCarbone M, Duty S and Rattray M (2012) Riluzole neuroprotection in a parkinson’s disease model involves suppression of reactive astrocytosis but not GLT-1 regulation. BMC Neuroscience, 13: 38.en_US
dc.identifier.urihttp://hdl.handle.net/10454/7807
dc.descriptionyesen_US
dc.description.abstractBackground: Riluzole is a neuroprotective drug used in the treatment of motor neurone disease. Recent evidence suggests that riluzole can up-regulate the expression and activity of the astrocyte glutamate transporter, GLT-1. Given that regulation of glutamate transport is predicted to be neuroprotective in Parkinson’s disease, we tested the effect of riluzole in parkinsonian rats which had received a unilateral 6-hydroxydopamine injection into the median forebrain bundle. Results: Rats were treated with intraperitoneal riluzole (4 mg/kg or 8 mg/kg), 1 hour before the lesion then once daily for seven days. Riluzole produced a modest but significant attenuation of dopamine neurone degeneration, assessed by suppression of amphetamine-induced rotations, preservation of tyrosine hydroxylase positive neuronal cell bodies in the substantia nigra pars compacta and attenuation of striatal tyrosine hydroxylase protein loss. Seven days after 6-hydroxydopamine lesion, reactive astrocytosis was observed in the striatum, as determined by increases in expression of glial fibrillary acidic protein, however the glutamate transporter, GLT-1, which is also expressed in astrocytes was not regulated by the lesion. Conclusions: The results confirm that riluzole is a neuroprotective agent in a rodent model of parkinson’s disease. Riluzole administration did not regulate GLT-1 levels but significantly reduced GFAP levels, in the lesioned striatum. Riluzole suppression of reactive astrocytosis is an intriguing finding which might contribute to the neuroprotective effects of this drug.en_US
dc.language.isoenen_US
dc.relation.isreferencedbyhttp://doi.org/10.1186/1471-2202-13-38en_US
dc.rights© 2012 Carbone et al. Published Open Access by BioMed Central. Reproduced in accordance with the publisher's self-archiving policy.en_US
dc.subjectRiluzole, EAAT2, GLT-1, Neuroprotection, Parkinson’s Disease, GFAP, Glial cell, 6-hydroxydopamineen_US
dc.titleRiluzole neuroprotection in a parkinson’s disease model involves suppression of reactive astrocytosis but not GLT-1 regulation.en_US
dc.status.refereedyesen_US
dc.typeArticleen_US
dc.type.versionpublished version paperen_US
refterms.dateFOA2018-07-25T14:18:02Z


Item file(s)

Thumbnail
Name:
art_Riluzole_10.1186_1471-2202 ...
Size:
439.2Kb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record