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Article: Electroacupuncture suppresses spinal expression of neurokinin-1 receptors induced by persistent inflammation in rats

TitleElectroacupuncture suppresses spinal expression of neurokinin-1 receptors induced by persistent inflammation in rats
Authors
KeywordsAcupuncture
Complete Freund's adjuvant
Hyperalgesia
Inflammatory pain
Neurokinin-1 receptor
Spinal cord
Issue Date2005
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2005, v. 384 n. 3, p. 339-343 How to Cite?
AbstractIt has been demonstrated that electroacupuncture (EA) significantly suppresses behavioral hyperalgesia in a rat model of persistent inflammatory pain and that neurokinin-1 (NK-1)/substance P (SP) receptors play important roles in nociception and hyperalgesia at the spinal cord level. The present study investigated spinal NK-1 receptor involvement in EA-produced suppression of hyperalgesia in a rat model of persistent inflammatory pain. The results showed that hind paw inflammation induced a significant increase of NK-1 receptor expression in the spinal dorsal horn and that this effect was significantly suppressed by EA. This suggests that EA-induced suppression of hyperalgesia is involved, at least partly, in the suppression of the spinal NK-1 receptors induced by sustained peripheral nociceptive input. © 2005 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188572
ISSN
2021 Impact Factor: 3.197
2020 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, RXen_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorQiao, JTen_US
dc.contributor.authorWang, Len_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:21Z-
dc.date.available2013-09-03T04:10:21Z-
dc.date.issued2005en_US
dc.identifier.citationNeuroscience Letters, 2005, v. 384 n. 3, p. 339-343en_US
dc.identifier.issn0304-3940en_US
dc.identifier.urihttp://hdl.handle.net/10722/188572-
dc.description.abstractIt has been demonstrated that electroacupuncture (EA) significantly suppresses behavioral hyperalgesia in a rat model of persistent inflammatory pain and that neurokinin-1 (NK-1)/substance P (SP) receptors play important roles in nociception and hyperalgesia at the spinal cord level. The present study investigated spinal NK-1 receptor involvement in EA-produced suppression of hyperalgesia in a rat model of persistent inflammatory pain. The results showed that hind paw inflammation induced a significant increase of NK-1 receptor expression in the spinal dorsal horn and that this effect was significantly suppressed by EA. This suggests that EA-induced suppression of hyperalgesia is involved, at least partly, in the suppression of the spinal NK-1 receptors induced by sustained peripheral nociceptive input. © 2005 Elsevier Ireland Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_US
dc.relation.ispartofNeuroscience Lettersen_US
dc.subjectAcupuncture-
dc.subjectComplete Freund's adjuvant-
dc.subjectHyperalgesia-
dc.subjectInflammatory pain-
dc.subjectNeurokinin-1 receptor-
dc.subjectSpinal cord-
dc.subject.meshAnimalsen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshElectroacupuncture - Methodsen_US
dc.subject.meshFreund's Adjuvanten_US
dc.subject.meshHyperalgesia - Etiology - Metabolism - Therapyen_US
dc.subject.meshInflammation - Chemically Induced - Metabolism - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Neurokinin-1 - Metabolismen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.subject.meshTreatment Outcomeen_US
dc.titleElectroacupuncture suppresses spinal expression of neurokinin-1 receptors induced by persistent inflammation 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.neulet.2005.05.001en_US
dc.identifier.pmid15908113-
dc.identifier.scopuseid_2-s2.0-20644445418en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20644445418&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume384en_US
dc.identifier.issue3en_US
dc.identifier.spage339en_US
dc.identifier.epage343en_US
dc.identifier.isiWOS:000230463700026-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridLiu, B=55720712900en_US
dc.identifier.scopusauthoridQiao, JT=7103301572en_US
dc.identifier.scopusauthoridWang, L=9036448600en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.issnl0304-3940-

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