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Article: Electroacupuncture inhibition of hyperalgesia in an inflammatory pain rat model: Involvement of distinct spinal serotonin and norepinephrine receptor subtypes

TitleElectroacupuncture inhibition of hyperalgesia in an inflammatory pain rat model: Involvement of distinct spinal serotonin and norepinephrine receptor subtypes
Authors
Issue Date2012
PublisherOxford University Press. The Journal's web site is located at http://bja.oxfordjournals.org/
Citation
British Journal Of Anaesthesia, 2012, v. 109 n. 2, p. 245-252 How to Cite?
AbstractBackground Although acupuncture analgesia is well documented, its mechanisms have not been thoroughly clarified. We previously showed that electroacupuncture (EA) activates supraspinal serotonin- and norepinephrine-containing neurones that project to the spinal cord. This study investigates the involvement of spinal alpha(2)-adrenoceptors (α2-ARs) and 5-hydroxytryptamine (serotonin) receptors (5-HTRs) in EA effects on an inflammatory pain rat model.MethodsInflammatory hyperalgesia was induced by injecting complete Freund's adjuvant (CFA, 0.08 ml) into the plantar surface of one hind paw and assessed by paw withdrawal latency (PWL) to a noxious thermal stimulus. The selective α2a-AR antagonist BRL-44408, α2b-AR antagonist imiloxan hydrochloride, 5-HT2B receptor (5-HT2BR) antagonist SB204741, 5-HT3R antagonist LY278584, or 5-HT1AR antagonists NAN-190 hydrobromide, or WAY-100635 were intrathecally administered 20 min before EA or sham EA, which was given 2 h post-CFA at acupoint GB30.ResultsEA significantly increased PWL compared with sham [7.20 (0.46) vs 5.20 (0.43) s]. Pretreatment with α2a-AR [5.35 (0.45) s] or 5-HT1AR [5.22 (0.38) s] antagonists blocked EA-produced anti-hyperalgesia; α2b-AR, 5-HT2BR, and 5-HT3R antagonist pretreatment did not. Sham plus these antagonists did not significantly change PWL compared with sham plus vehicle, indicating that the antagonists had little effect on PWL. Immunohistochemical staining demonstrated that α2a-ARs are on primary afferents and 5-HT1ARs are localized in N-methyl-d-aspartic acid (NMDA) subunit NR1-containing neurones in the spinal dorsal horn.ConclusionsThe data show that α2a-ARs and 5-HT1ARs are involved in the EA inhibition of inflammatory pain and that the NMDA receptors are involved in EA action. © The Author [2012]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissionsoup.com2012 © © The Author [2012]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188653
ISSN
2015 Impact Factor: 5.616
2015 SCImago Journal Rankings: 2.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_US
dc.contributor.authorZhang, RXen_US
dc.contributor.authorZhang, Men_US
dc.contributor.authorShen, XYen_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorXin, Jen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorTan, Men_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:52Z-
dc.date.available2013-09-03T04:10:52Z-
dc.date.issued2012en_US
dc.identifier.citationBritish Journal Of Anaesthesia, 2012, v. 109 n. 2, p. 245-252en_US
dc.identifier.issn0007-0912en_US
dc.identifier.urihttp://hdl.handle.net/10722/188653-
dc.description.abstractBackground Although acupuncture analgesia is well documented, its mechanisms have not been thoroughly clarified. We previously showed that electroacupuncture (EA) activates supraspinal serotonin- and norepinephrine-containing neurones that project to the spinal cord. This study investigates the involvement of spinal alpha(2)-adrenoceptors (α2-ARs) and 5-hydroxytryptamine (serotonin) receptors (5-HTRs) in EA effects on an inflammatory pain rat model.MethodsInflammatory hyperalgesia was induced by injecting complete Freund's adjuvant (CFA, 0.08 ml) into the plantar surface of one hind paw and assessed by paw withdrawal latency (PWL) to a noxious thermal stimulus. The selective α2a-AR antagonist BRL-44408, α2b-AR antagonist imiloxan hydrochloride, 5-HT2B receptor (5-HT2BR) antagonist SB204741, 5-HT3R antagonist LY278584, or 5-HT1AR antagonists NAN-190 hydrobromide, or WAY-100635 were intrathecally administered 20 min before EA or sham EA, which was given 2 h post-CFA at acupoint GB30.ResultsEA significantly increased PWL compared with sham [7.20 (0.46) vs 5.20 (0.43) s]. Pretreatment with α2a-AR [5.35 (0.45) s] or 5-HT1AR [5.22 (0.38) s] antagonists blocked EA-produced anti-hyperalgesia; α2b-AR, 5-HT2BR, and 5-HT3R antagonist pretreatment did not. Sham plus these antagonists did not significantly change PWL compared with sham plus vehicle, indicating that the antagonists had little effect on PWL. Immunohistochemical staining demonstrated that α2a-ARs are on primary afferents and 5-HT1ARs are localized in N-methyl-d-aspartic acid (NMDA) subunit NR1-containing neurones in the spinal dorsal horn.ConclusionsThe data show that α2a-ARs and 5-HT1ARs are involved in the EA inhibition of inflammatory pain and that the NMDA receptors are involved in EA action. © The Author [2012]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissionsoup.com2012 © © The Author [2012]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://bja.oxfordjournals.org/en_US
dc.relation.ispartofBritish Journal of Anaesthesiaen_US
dc.subject.meshAdrenergic Alpha-2 Receptor Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshElectroacupuncture - Methodsen_US
dc.subject.meshFreund's Adjuvanten_US
dc.subject.meshHot Temperatureen_US
dc.subject.meshHyperalgesia - Chemically Induced - Metabolism - Prevention & Controlen_US
dc.subject.meshMaleen_US
dc.subject.meshPain Measurement - Methodsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReaction Time - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Adrenergic, Alpha-2 - Metabolism - Physiologyen_US
dc.subject.meshReceptors, Serotonin, 5-Ht1 - Metabolism - Physiologyen_US
dc.subject.meshSerotonin 5-Ht1 Receptor Antagonists - Pharmacologyen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.titleElectroacupuncture inhibition of hyperalgesia in an inflammatory pain rat model: Involvement of distinct spinal serotonin and norepinephrine receptor subtypesen_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.doi10.1093/bja/aes136en_US
dc.identifier.pmid22628394-
dc.identifier.scopuseid_2-s2.0-84863966371en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863966371&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume109en_US
dc.identifier.issue2en_US
dc.identifier.spage245en_US
dc.identifier.epage252en_US
dc.identifier.isiWOS:000306363900018-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridZhang, Y=55316213200en_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridZhang, M=36041252700en_US
dc.identifier.scopusauthoridShen, XY=7402721090en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridXin, J=23104505000en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridTan, M=55127194900en_US
dc.identifier.scopusauthoridLao, L=55314564300en_US

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