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dc.contributor.authorBezard, Erwan-
dc.contributor.authorGerlach, I.-
dc.contributor.authorMoratalla, Rosario-
dc.contributor.authorGross, C. E.-
dc.contributor.authorJork, R.-
dc.date.accessioned2012-11-06T11:54:06Z-
dc.date.available2012-11-06T11:54:06Z-
dc.date.issued2006-
dc.identifierdoi: 10.1016/j.nbd.2006.02.003-
dc.identifierissn: 0969-9961-
dc.identifier.citationNeurobiology of Disease 23: 77- 86 (2006)-
dc.identifier.urihttp://hdl.handle.net/10261/59551-
dc.description.abstractExcitotoxicity-mediated cell death is involved in Parkinson's disease (PD). 5-HT1A receptor agonists can protect from such mechanisms. The current study demonstrates that the 5-HT1A agonists BAY 639044 and repinotan have neuroprotective effects in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In addition, we also show that both compounds delay the appearance of parkinsonian motor abnormalities in a MPTP monkey model that recapitulates the progressive nature of PD. Thus, BAY 639044 or repinotan treatment was initiated when there was 30% neuronal death in the substantia nigra pars compacta, and nerve terminal loss in the striatum was 40%, i.e., compatible with the clinical situation where early symptomatic patients would receive such a treatment. The delay in appearance of parkinsonian motor abnormalities is a consequence of partial neuroprotection of nigrostriatal dopamine neurons, both at neuronal and terminal levels as shown for BAY 639044. These results suggest that 5-HT1A agonists, such as BAY 639044, may protect from neurodegeneration and delay the worsening of motor symptoms in Parkinson patients. © 2006.-
dc.language.isoeng-
dc.publisherAcademic Press-
dc.rightsclosedAccess-
dc.title5-HT1A receptor agonist-mediated protection from MPTP toxicity in mouse and macaque models of Parkinson's disease-
dc.typeartículo-
dc.identifier.doihttp://dx.doi.org/10.1016/j.nbd.2006.02.003-
dc.date.updated2012-11-06T11:54:07Z-
dc.description.versionPeer Reviewed-
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