Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson's disease.

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dc.contributor.author Collins, Louise M.
dc.contributor.author Gavin, Aisling M.
dc.contributor.author Walsh, Sinéad
dc.contributor.author Sullivan, Aideen M.
dc.contributor.author Wyatt, Sean L.
dc.contributor.author O'Keeffe, Gerard W.
dc.contributor.author Nolan, Yvonne M.
dc.contributor.author Toulouse, André
dc.date.accessioned 2014-08-12T13:57:22Z
dc.date.available 2014-08-12T13:57:22Z
dc.date.issued 2014-05
dc.identifier.citation COLLINS, L. M., GAVIN, A. M., WALSH, S., SULLIVAN, A. M., WYATT, S. L., O'KEEFFE, G. W., NOLAN, Y. M. & TOULOUSE, A. 2014. Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson's disease. SpringerPlus, 3, 205. doi: 10.1186/2193-1801-3-205 en
dc.identifier.volume 3 en
dc.identifier.issued 1 en
dc.identifier.startpage 205 en
dc.identifier.endpage 205 en
dc.identifier.uri http://hdl.handle.net/10468/1616
dc.identifier.doi 10.1186/2193-1801-3-205
dc.description.abstract We have previously demonstrated that mitogen-activated protein kinase phosphatase 1, Mkp1, is expressed in the developing and rat adult substantia nigra and striatum, where it promotes the growth of nigral dopaminergic neurons. Mkp1 may therefore have therapeutic potential for Parkinson's disease. In the present study, we have assessed the expression of Mkp1 and TH in the substantia nigra and striatum of parkinsonian rat models. Expression was measured at 4 and 10 days post-lesion in the 6-hydroxydopamine (6-OHDA) medial forebrain bundle lesion model and after 4, 10 and 28 days in the 6-OHDA striatal lesion model. Our results show that Mkp1 expression was transiently up-regulated in the substantia nigra at 4 days post-6-OHDA administration in the two models while TH expression was decreased at the later time-points examined. These data suggest that Mkp1 may play a role in counteracting the neurotoxic effects of 6-OHDA in nigral dopaminergic neurons. en
dc.description.sponsorship Health Research Board (HRA/2009/127); Science Foundation Ireland (Grant No. SFI/RFP/NSC1298) (10/RFP/NES5786) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Springer en
dc.relation.uri http://www.springerplus.com/content/3/1/205
dc.rights © 2014 Collins et al.; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited en
dc.rights.uri http://creativecommons.org/licenses/by/4.0 en
dc.subject Parkinson’s disease en
dc.subject 6-hydroxydopamine en
dc.subject MAP kinase phosphatase 1 (Mkp1) en
dc.title Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson's disease. en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother André Toulouse, Department Of Anatomy & Neuroscience, University College Cork, Cork, Ireland. +353-21-490-3000 Email: a.toulouse@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2014-05-14T13:30:10Z
dc.description.version Published Version en
dc.internal.rssid 253781800
dc.contributor.funder Health Research Board en
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder College of Medicine and Health, University College Cork
dc.description.status Peer reviewed en
dc.identifier.journaltitle SpringerPlus en
dc.internal.copyrightchecked No. Open ACcess - PV permitted. CC-BY licence en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress a.toulouse@ucc.ie en


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© 2014 Collins et al.; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited Except where otherwise noted, this item's license is described as © 2014 Collins et al.; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited
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