Neuroprotective effect of riluzole in a primate model of Parkinson's disease: behavioral and histological evidence.
Identifieur interne : 001217 ( PubMed/Corpus ); précédent : 001216; suivant : 001218Neuroprotective effect of riluzole in a primate model of Parkinson's disease: behavioral and histological evidence.
Auteurs : Maria C. Obinu ; Michel Reibaud ; Véronique Blanchard ; Saliha Moussaoui ; Assunta ImperatoSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2002.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animals, Behavior, Animal (drug effects), Callithrix, Disease Models, Animal, Dopamine (metabolism), Dopamine Agents (adverse effects), Female, Immunohistochemistry, Locomotion (drug effects), Male, Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Nissl Bodies (drug effects), Nissl Bodies (metabolism), Nissl Bodies (pathology), Parkinson Disease (drug therapy), Parkinson Disease, Secondary (chemically induced), Random Allocation, Riluzole (pharmacology), Riluzole (therapeutic use), Substantia Nigra (drug effects).
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Behavior, Animal, Locomotion, Nissl Bodies, Substantia Nigra.
- drug therapy : Parkinson Disease.
- chemical , metabolism : Dopamine, Nissl Bodies.
- pathology : Nissl Bodies.
- chemical , pharmacology : Neuroprotective Agents, Riluzole.
- chemical , therapeutic use : Neuroprotective Agents, Riluzole.
- Animals, Callithrix, Disease Models, Animal, Female, Immunohistochemistry, Male, Random Allocation.
Abstract
Our study aimed to determine whether riluzole, which has shown efficacy as a disease-modifying agent in amyotrophic lateral sclerosis (ALS), is neuroprotective in a marmoset model of Parkinson's disease (PD). Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP-induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH- and Nissl-stained nigral neurons and of TH-stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. We conclude that riluzole protects dopaminergic neurons and reduces behavioral deficits in a marmoset model of PD.
PubMed: 11835434
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Marie-Carmen.Obinu@aventis.com</nlm:affiliation></affiliation></author><author><name sortKey="Reibaud, Michel" sort="Reibaud, Michel" uniqKey="Reibaud M" first="Michel" last="Reibaud">Michel Reibaud</name></author><author><name sortKey="Blanchard, Veronique" sort="Blanchard, Veronique" uniqKey="Blanchard V" first="Véronique" last="Blanchard">Véronique Blanchard</name></author><author><name sortKey="Moussaoui, Saliha" sort="Moussaoui, Saliha" uniqKey="Moussaoui S" first="Saliha" last="Moussaoui">Saliha Moussaoui</name></author><author><name sortKey="Imperato, Assunta" sort="Imperato, Assunta" uniqKey="Imperato A" first="Assunta" last="Imperato">Assunta Imperato</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:11835434</idno><idno type="pmid">11835434</idno><idno type="wicri:Area/PubMed/Corpus">001217</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001217</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroprotective effect of riluzole in a primate model of Parkinson's disease: behavioral and histological evidence.</title><author><name sortKey="Obinu, Maria C" sort="Obinu, Maria C" uniqKey="Obinu M" first="Maria C" last="Obinu">Maria C. Obinu</name><affiliation><nlm:affiliation>Neurodegenerative Disease Program, Research Center of Paris, Aventis Pharma, S.A. Vitry sur Seine, France. 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Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP-induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH- and Nissl-stained nigral neurons and of TH-stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. We conclude that riluzole protects dopaminergic neurons and reduces behavioral deficits in a marmoset model of PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11835434</PMID><DateCreated><Year>2002</Year><Month>02</Month><Day>08</Day></DateCreated><DateCompleted><Year>2002</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>17</Volume><Issue>1</Issue><PubDate><Year>2002</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neuroprotective effect of riluzole in a primate model of Parkinson's disease: behavioral and histological evidence.</ArticleTitle><Pagination><MedlinePgn>13-9</MedlinePgn></Pagination><Abstract><AbstractText>Our study aimed to determine whether riluzole, which has shown efficacy as a disease-modifying agent in amyotrophic lateral sclerosis (ALS), is neuroprotective in a marmoset model of Parkinson's disease (PD). Reduction of energy demand by riluzole could be a rational neuroprotective strategy with good tolerability. The efficacy of riluzole was evaluated in marmosets by testing its ability to reduce MPTP-induced behavioral deficits and loss of dopaminergic nigral neurons. Marmosets were divided into two groups of four animals each: animals in Group 1 were injected twice with MPTP (2 mg/kg subcutaneous) and treated with riluzole (10 mg/kg per os b.i.d.), animals in Group 2 (controls) were injected with MPTP and with the vehicle of riluzole. A third group of marmosets which did not receive MPTP or riluzole drug was introduced for neurohistopathological studies (normal animals). Marmosets treated with riluzole preserved a better motor function and neurological performance through the 26 days of assessment when compared with the controls. Histologically, there was sparing of TH- and Nissl-stained nigral neurons and of TH-stained terminals in the striatum and the putamen in the group treated with riluzole compared to the controls. 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