Riluzole neuroprotection in a parkinson’s disease model involves suppression of reactive astrocytosis but not GLT-1 regulation.
dc.contributor.author | Carbone, M. | * |
dc.contributor.author | Duty, S. | * |
dc.contributor.author | Rattray, Marcus | * |
dc.date.accessioned | 2016-02-23T16:28:40Z | |
dc.date.available | 2016-02-23T16:28:40Z | |
dc.date.issued | 2012-04 | |
dc.identifier.citation | Carbone 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. | |
dc.identifier.uri | http://hdl.handle.net/10454/7807 | |
dc.description | Yes | |
dc.description.abstract | Background: 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. | |
dc.language.iso | en | |
dc.rights | © 2012 Carbone et al. Published Open Access by BioMed Central. Reproduced in accordance with the publisher's self-archiving policy. | |
dc.subject | Riluzole | |
dc.subject | EAAT2 | |
dc.subject | GLT-1 | |
dc.subject | Neuroprotection | |
dc.subject | Parkinson’s Disease | |
dc.subject | GFAP | |
dc.subject | Glial cell | |
dc.subject | 6-hydroxydopamine | |
dc.title | Riluzole neuroprotection in a parkinson’s disease model involves suppression of reactive astrocytosis but not GLT-1 regulation. | |
dc.status.refereed | Yes | |
dc.type | Article | |
dc.type.version | Published version | |
dc.identifier.doi | https://doi.org/10.1186/1471-2202-13-38 | |
dc.rights.license | Unspecified | |
refterms.dateFOA | 2018-07-25T14:18:02Z | |
dc.openaccess.status | openAccess |