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dc.contributor.authorJones, NC
dc.contributor.authorPrior, MJW
dc.contributor.authorBurden-Teh, E
dc.contributor.authorMarsden, CA
dc.contributor.authorMorris, PG
dc.contributor.authorMurphy, S
dc.date.available2014-05-21T19:26:33Z
dc.date.issued2005-07-01
dc.identifierpii: EJN4221
dc.identifier.citationJones, N. C., Prior, M. J. W., Burden-Teh, E., Marsden, C. A., Morris, P. G. & Murphy, S. (2005). Antagonism of the interleukin-1 receptor following traumatic brain injury in the mouse reduces the number of nitric oxide synthase-2-positive cells and improves anatomical and functional outcomes. EUROPEAN JOURNAL OF NEUROSCIENCE, 22 (1), pp.72-78. https://doi.org/10.1111/j.1460-9568.2005.04221.x.
dc.identifier.issn0953-816X
dc.identifier.urihttp://hdl.handle.net/11343/26291
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractInterleukin (IL)-1beta plays an important role in the inflammatory response that results from traumatic brain injury and antagonism of the actions of this cytokine can affect outcome. We subjected male mice to aseptic cryogenic injury and assessed recovery through anatomical, histological and functional measures following treatment with recombinant mouse IL-1 receptor antagonist (IL-1ra). A single dose (1 microg, i.c.v.) at the time of injury reduced lesion volume 3 days later, as assessed by Nissl staining, and also the number (30%) of FluoroJade-positive degenerating neurones. Mice treated with IL-1ra performed better on the beam balance and in the grid test as compared with vehicle-treated animals. Furthermore, IL-1ra-treated animals showed fewer (40%) nitric oxide synthase-2-positive cells in and around the lesion. These data suggest that activation of the IL-1 receptor following trauma contributes to the pathology and that antagonism can reduce both anatomical and functional consequences of neuroinflammation.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherWILEY
dc.subjectCentral Nervous System ; Nervous System and Disorders
dc.titleAntagonism of the interleukin-1 receptor following traumatic brain injury in the mouse reduces the number of nitric oxide synthase-2-positive cells and improves anatomical and functional outcomes
dc.typeJournal Article
dc.identifier.doi10.1111/j.1460-9568.2005.04221.x
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMedicine - Royal Melbourne And Western Hospitals
melbourne.source.titleEUROPEAN JOURNAL OF NEUROSCIENCE
melbourne.source.volume22
melbourne.source.issue1
melbourne.source.pages72-78
melbourne.publicationid74771
melbourne.elementsid286623
melbourne.contributor.authorJones, Nigel
dc.identifier.eissn1460-9568
melbourne.accessrightsThis item is currently not available from this repository


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