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Article: IL-1ra alleviates inflammatory hyperalgesia through preventing phosphorylation of NMDA receptor NR-1 subunit in rats

TitleIL-1ra alleviates inflammatory hyperalgesia through preventing phosphorylation of NMDA receptor NR-1 subunit in rats
Authors
Issue Date2008
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/pain
Citation
Pain, 2008, v. 135 n. 3, p. 232-239 How to Cite?
AbstractAlthough it has been shown that pro-inflammatory cytokines such as interleukin-1β (IL-1β) facilitate perception of noxious inputs at the spinal level, the mechanisms have not been understood. This study determined the cell type that produces IL-1β, the co-localization of IL-1 receptor type I (IL-1RI) and Fos and NR1 in the spinal cord, and the effects of IL-1 receptor antagonist (IL-1ra) on NR1 phosphorylation and hyperalgesia in a rat model of inflammatory pain. Phosphorylation of NR1, an essential subunit of the NMDA receptor (NMDAR), is known to modulate NMDAR activity and facilitate pain. Hyperalgesia was induced by injecting complete Freund's adjuvant (CFA, 0.08 ml, 40 μg Mycobacterium tuberculosis) into one hind paw of each rat. Paw withdrawal latency (PWL) was tested before CFA (-48 h) for baseline and 2 and 24 h after CFA to assess hyperalgesia. IL-1ra was given (i.t.) 24 h before CFA to block the action of basal IL-1β and 2 h prior to each of two PWL tests to block CFA-induced IL-1β. Spinal cords were removed for double immunostaining of IL-1β/neuronal marker and IL-1β/glial cell markers, IL-1RI/Fos and IL-1RI/NR1, and for Western blot to measure NR1 phosphorylation. The data showed that: (1) astrocytes produce IL-1β, (2) IL-1RI is localized in Fos- and NR1-immunoreactive neurons within the spinal dorsal horn, and (3) IL-1ra at 0.01 mg/rat significantly increased PWL (P < 0.05) and inhibited NR1 phosphorylation compared to saline control. The results suggest that spinal IL-1β is produced by astrocytes and enhances NR1 phosphorylation to facilitate inflammatory pain. © 2007 International Association for the Study of Pain.
Persistent Identifierhttp://hdl.handle.net/10722/188594
ISSN
2015 Impact Factor: 5.557
2015 SCImago Journal Rankings: 3.007
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, RXen_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorWang, Len_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorZhang, Hen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:29Z-
dc.date.available2013-09-03T04:10:29Z-
dc.date.issued2008en_US
dc.identifier.citationPain, 2008, v. 135 n. 3, p. 232-239en_US
dc.identifier.issn0304-3959en_US
dc.identifier.urihttp://hdl.handle.net/10722/188594-
dc.description.abstractAlthough it has been shown that pro-inflammatory cytokines such as interleukin-1β (IL-1β) facilitate perception of noxious inputs at the spinal level, the mechanisms have not been understood. This study determined the cell type that produces IL-1β, the co-localization of IL-1 receptor type I (IL-1RI) and Fos and NR1 in the spinal cord, and the effects of IL-1 receptor antagonist (IL-1ra) on NR1 phosphorylation and hyperalgesia in a rat model of inflammatory pain. Phosphorylation of NR1, an essential subunit of the NMDA receptor (NMDAR), is known to modulate NMDAR activity and facilitate pain. Hyperalgesia was induced by injecting complete Freund's adjuvant (CFA, 0.08 ml, 40 μg Mycobacterium tuberculosis) into one hind paw of each rat. Paw withdrawal latency (PWL) was tested before CFA (-48 h) for baseline and 2 and 24 h after CFA to assess hyperalgesia. IL-1ra was given (i.t.) 24 h before CFA to block the action of basal IL-1β and 2 h prior to each of two PWL tests to block CFA-induced IL-1β. Spinal cords were removed for double immunostaining of IL-1β/neuronal marker and IL-1β/glial cell markers, IL-1RI/Fos and IL-1RI/NR1, and for Western blot to measure NR1 phosphorylation. The data showed that: (1) astrocytes produce IL-1β, (2) IL-1RI is localized in Fos- and NR1-immunoreactive neurons within the spinal dorsal horn, and (3) IL-1ra at 0.01 mg/rat significantly increased PWL (P < 0.05) and inhibited NR1 phosphorylation compared to saline control. The results suggest that spinal IL-1β is produced by astrocytes and enhances NR1 phosphorylation to facilitate inflammatory pain. © 2007 International Association for the Study of Pain.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/painen_US
dc.relation.ispartofPainen_US
dc.subject.meshAnalgesics - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents - Pharmacologyen_US
dc.subject.meshAstrocytes - Drug Effects - Immunologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshGliosis - Drug Therapy - Immunology - Physiopathologyen_US
dc.subject.meshHyperalgesia - Drug Therapy - Immunology - Physiopathologyen_US
dc.subject.meshInflammation - Drug Therapy - Immunology - Physiopathologyen_US
dc.subject.meshInflammation Mediators - Pharmacologyen_US
dc.subject.meshInterleukin 1 Receptor Antagonist Protein - Pharmacologyen_US
dc.subject.meshInterleukin-1Beta - Antagonists & Inhibitors - Immunologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPain - Drug Therapy - Immunology - Physiopathologyen_US
dc.subject.meshPain Threshold - Drug Effects - Physiologyen_US
dc.subject.meshPhosphorylation - Drug Effectsen_US
dc.subject.meshPosterior Horn Cells - Drug Effects - Immunology - Physiopathologyen_US
dc.subject.meshProto-Oncogene Proteins C-Fos - Drug Effects - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReaction Time - Drug Effects - Immunologyen_US
dc.subject.meshReceptors, Interleukin-1 - Antagonists & Inhibitors - Immunologyen_US
dc.subject.meshReceptors, N-Methyl-D-Aspartate - Drug Effects - Metabolismen_US
dc.titleIL-1ra alleviates inflammatory hyperalgesia through preventing phosphorylation of NMDA receptor NR-1 subunit in ratsen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.pain.2007.05.023en_US
dc.identifier.pmid17689191-
dc.identifier.scopuseid_2-s2.0-40049094003en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-40049094003&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume135en_US
dc.identifier.issue3en_US
dc.identifier.spage232en_US
dc.identifier.epage239en_US
dc.identifier.isiWOS:000254912700005-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridLiu, B=55720712900en_US
dc.identifier.scopusauthoridWang, L=9036448600en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridZhang, H=51563012400en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US

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