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dc.contributor.authorIravani, Mahmoud M.
dc.contributor.authorSadeghian, Mona
dc.contributor.authorLeung, Clement C. M.
dc.contributor.authorTel, Banu C.
dc.contributor.authorRose, Sarah
dc.contributor.authorSchapira, Anthony H.
dc.contributor.authorJenner, Peter
dc.date.accessioned2013-01-11T12:29:21Z
dc.date.available2013-01-11T12:29:21Z
dc.date.issued2008-08
dc.identifier.citationIravani , M M , Sadeghian , M , Leung , C C M , Tel , B C , Rose , S , Schapira , A H & Jenner , P 2008 , ' Continuous subcutaneous infusion of pramipexole protects against lipopolysaccharide-induced dopaminergic cell death without affecting the inflammatory response ' , Experimental Neurology , vol. 212 , no. 2 , pp. 522-531 . https://doi.org/10.1016/j.expneurol.2008.04.037
dc.identifier.issn0014-4886
dc.identifier.otherPURE: 735021
dc.identifier.otherPURE UUID: b1f63081-dac9-4cad-9705-3e35c275af64
dc.identifier.otherWOS: 000258252000035
dc.identifier.otherScopus: 47349086173
dc.identifier.otherORCID: /0000-0002-4905-9682/work/32997579
dc.identifier.urihttp://hdl.handle.net/2299/9570
dc.description.abstractThe D2/D3 dopamine receptor agonist pramipexole, protects against toxin-induced dopaminergic neuronal destruction but its mechanism of action is unknown. Inflammation following glial cell activation contributes to cell death in Parkinson's disease and we now report on the effects of acute or chronic administration of pramipexole on lipopolysaccharide (LPS) induced inflammation and nigral dopaminergic cell death in the rat. At 48 h and 30 days following supranigral administration of LPS, approximately 70% of tyrosine hydroxylase (TH) immunoreactive (-ir) cells in substantia nigra had degenerated with a corresponding loss of TH-ir terminals in the striatum. In rats acutely treated with pramipexole (2 x 1 mg/k; s.c.) 48 h following LPS application, there was no difference in the number of TH-ir cells or terminals compared to LPS-treated Fats receiving vehicle. However, the continuous Subcutaneous infusion of pramipexole for 7 days prior to LPS and 21 days subsequently, produced a marked preservation of both TH-ir cells and terminals. At 48 h or 30 days, LPS induced an up-regulation of ubiquitin-ir within the nigral TH-ir neurons, which was reduced by pramipexole treatment. Thirty days following supranigral LPS administration (9 days after the end of infusion), (+)-amphetamine (5 mg/kg, i.p.) caused robust ipsiversive rotation. In rats treated with LPS but receiving continuous subcutaneous administration of pramipexole, (+)-amphetamine-induced rotation was markedly reduced. LPS-induced increase in the levels of inflammatory markers, were not affected by either acute administration or Continuous infusion of pramipexole. Continuous infusion of pramipexole protected dopaminergic neurones against inflammation induced degeneration but without modification of the inflammatory response. (C) 2008 Elsevier Inc. All rights reserved.en
dc.format.extent10
dc.language.isoeng
dc.relation.ispartofExperimental Neurology
dc.subjectlipopolysaccharide
dc.subjectpramipexole
dc.subjectsubstantia nigra
dc.subjectstriatum
dc.subjectinducible nitric oxide synthase (iNOS)
dc.subjectglial cells
dc.subjectParkinson's disease
dc.subjectINHIBITS LIPID-PEROXIDATION
dc.subjectPARKINSONS-DISEASE
dc.subjectAGONIST PRAMIPEXOLE
dc.subjectIN-VITRO
dc.subjectFREE-RADICALS
dc.subjectRAT-BRAIN
dc.subjectINDUCED NEUROTOXICITY
dc.subjectRECEPTOR AGONISTS
dc.subjectSUBSTANTIA-NIGRA
dc.subjectPRIMARY CULTURE
dc.titleContinuous subcutaneous infusion of pramipexole protects against lipopolysaccharide-induced dopaminergic cell death without affecting the inflammatory responseen
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionPharmacology and Clinical Science Research
dc.contributor.institutionNeurodegenerative Diseases
dc.description.statusPeer reviewed
rioxxterms.versionVoR
rioxxterms.versionofrecordhttps://doi.org/10.1016/j.expneurol.2008.04.037
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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