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dc.contributor.authorIravani, Mahmoud M.
dc.contributor.authorLiu, L.
dc.contributor.authorRose, S.
dc.contributor.authorJenner, P.
dc.date.accessioned2013-06-24T08:00:53Z
dc.date.available2013-06-24T08:00:53Z
dc.date.issued2004-12-10
dc.identifier.citationIravani , M M , Liu , L , Rose , S & Jenner , P 2004 , ' Role of inducible nitric oxide synthase in N-methyl-D-aspartic acid-induced strio-nigral degeneration ' , Brain Research , vol. 1029 , no. 1 , pp. 103-113 . https://doi.org/10.1016/j.brainres.2004.09.033
dc.identifier.issn0006-8993
dc.identifier.otherPURE: 735600
dc.identifier.otherPURE UUID: 3b1e11fc-971b-4f7d-aa59-9e9a19aa8b2c
dc.identifier.otherWOS: 000225481700012
dc.identifier.otherScopus: 7744232267
dc.identifier.otherORCID: /0000-0002-4905-9682/work/32997593
dc.identifier.urihttp://hdl.handle.net/2299/10899
dc.description.abstractN-Methyl-D-aspartate (NMDA)-induced striatal excitotoxicity is mediated by nitric oxide (NO) but the role of inflammatory mechanisms and inducible nitric oxide synthase (iNOS) induction is not clear. Unilateral intrastriatal administration of NMDA to rats resulted in the loss of intrinsic striatal neurones and the degeneration of NADPH-diaphorase positive interneurones within 24 It. NMDA administration caused activation of glial fibrillary acidic protein positive astroglial cells and MAC-1 ir microglia. Marked iNOS immunoreactivity was expressed within both astroglial and microglial cells and there was marked cellular labelling for 3-nitrotyrosine (3-NT). One month following the NMDA lesion, administration of (+)-amphetamine (AMPH) produced a circling response in rats. Pre-treatment of rats with the iNOS inhibitor aminoguanidine (AG) decreased the extent of NMDA-induced striatal cell loss at 24 It and reduced 3-NT expression but was without effect on glial cell activation. AG pre-treatment also prevented the onset of rotation to AMPH at 3 0 days following NMDA lesioning. NMDA administration unexpectedly caused a loss of tyrosine hydroxylase immunoreactive (TH-ir) fibres in the striatum at 24 h and at 30 days the number of TH-ir cells were decreased in the substantia nigra. The loss of nigral cells was prevented by AG pre-treatment. This study demonstrates a role for iNOS induction in NO-mediated NMDA excitotoxicity to rat striatum and suggests that inflammatory mechanisms play a key role in this process. (C) 2004 Elsevier B.V. All rights reserved.en
dc.format.extent11
dc.language.isoeng
dc.relation.ispartofBrain Research
dc.subjectinflammation
dc.subjectnitric oxide
dc.subjectinducible nitric oxide synthase
dc.subjectN-methyl-D-aspartate
dc.subjectglia
dc.subjectTRANSIENT CEREBRAL-ISCHEMIA
dc.subjectEXCITOTOXIC BRAIN-DAMAGE
dc.subjectQUINOLINIC ACID
dc.subjectNEURONAL DEATH
dc.subjectRAT-BRAIN
dc.subject3-NITROPROPIONIC ACID
dc.subjectGLUTAMATE RECEPTORS
dc.subjectHUNTINGTONS-DISEASE
dc.subjectSTRIATAL NEURONS
dc.subjectINOS EXPRESSION
dc.titleRole of inducible nitric oxide synthase in N-methyl-D-aspartic acid-induced strio-nigral degenerationen
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.contributor.institutionAgriculture, Veterinary and Food Sciences
dc.description.statusPeer reviewed
rioxxterms.versionofrecordhttps://doi.org/10.1016/j.brainres.2004.09.033
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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