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Article: Rostral ventromedial medulla μ, but not κ, opioid receptors are involved in electroacupuncture anti-hyperalgesia in an inflammatory pain rat model

TitleRostral ventromedial medulla μ, but not κ, opioid receptors are involved in electroacupuncture anti-hyperalgesia in an inflammatory pain rat model
Authors
Issue Date2011
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 2011, v. 1395, p. 38-45 How to Cite?
AbstractIt has been reported that intracerebroventricular injection of a μ receptor antagonist blocked 2 but not 100 Hz electroacupuncture (EA)-produced analgesia in an uninjured animal model. Because persistent pain changes neural response to external stimulation, we hypothesized that the mechanisms of EA anti-hyperalgesia may be different in persistent pain than in health. Hyperalgesia, decreased paw withdrawal latency (PWL) to a noxious thermal stimulus, was induced by subcutaneously injecting complete Freund's adjuvant (CFA) into the hind paws of rats. Selective antagonists against μ (CTOP: D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-ThrNH2, 6.25 nmol) and κ (Nor-BIN: nor-binaltorphimine, 10 nmol) opioid receptors were infused into the rostral ventromedial medulla (RVM) 10 min before a 30-min EA treatment at acupoint Huantiao (GB30) 1 h 30 min post-CFA. PWL was measured before and 2.5 post-CFA. Both 10 Hz and 100 Hz EA-produced anti-hyperalgesia were blocked by intra-RVM μ, but not κ, receptor antagonists. Double immunofluorescence staining demonstrated that μ receptor-containing neurons were GABAnergic and that GABAa receptor-containing neurons were serotonergic in the RVM. The results demonstrated an involvement of RVM μ, but not κ, receptors in EA-produced anti-hyperalgesia. In summary, EA may induce release of endogenous endomorphins that activate μ opioid receptors in GABAnergic neurons to suppress the release of GABA. This removes the tonic inhibition of GABA on serotonergic neurons in the RVM, and activation of these serotonergic neurons inhibits pain. EA may be used as complementary treatment for inflammatory pain. © 2011 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188630
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorLao, Len_US
dc.contributor.authorXin, Jen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorZhang, RXen_US
dc.date.accessioned2013-09-03T04:10:43Z-
dc.date.available2013-09-03T04:10:43Z-
dc.date.issued2011en_US
dc.identifier.citationBrain Research, 2011, v. 1395, p. 38-45en_US
dc.identifier.issn0006-8993en_US
dc.identifier.urihttp://hdl.handle.net/10722/188630-
dc.description.abstractIt has been reported that intracerebroventricular injection of a μ receptor antagonist blocked 2 but not 100 Hz electroacupuncture (EA)-produced analgesia in an uninjured animal model. Because persistent pain changes neural response to external stimulation, we hypothesized that the mechanisms of EA anti-hyperalgesia may be different in persistent pain than in health. Hyperalgesia, decreased paw withdrawal latency (PWL) to a noxious thermal stimulus, was induced by subcutaneously injecting complete Freund's adjuvant (CFA) into the hind paws of rats. Selective antagonists against μ (CTOP: D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-ThrNH2, 6.25 nmol) and κ (Nor-BIN: nor-binaltorphimine, 10 nmol) opioid receptors were infused into the rostral ventromedial medulla (RVM) 10 min before a 30-min EA treatment at acupoint Huantiao (GB30) 1 h 30 min post-CFA. PWL was measured before and 2.5 post-CFA. Both 10 Hz and 100 Hz EA-produced anti-hyperalgesia were blocked by intra-RVM μ, but not κ, receptor antagonists. Double immunofluorescence staining demonstrated that μ receptor-containing neurons were GABAnergic and that GABAa receptor-containing neurons were serotonergic in the RVM. The results demonstrated an involvement of RVM μ, but not κ, receptors in EA-produced anti-hyperalgesia. In summary, EA may induce release of endogenous endomorphins that activate μ opioid receptors in GABAnergic neurons to suppress the release of GABA. This removes the tonic inhibition of GABA on serotonergic neurons in the RVM, and activation of these serotonergic neurons inhibits pain. EA may be used as complementary treatment for inflammatory pain. © 2011 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_US
dc.relation.ispartofBrain Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshElectroacupuncture - Methodsen_US
dc.subject.meshFreund's Adjuvant - Administration & Dosage - Toxicityen_US
dc.subject.meshHyperalgesia - Metabolism - Physiopathology - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshMedulla Oblongata - Drug Effects - Metabolism - Physiopathologyen_US
dc.subject.meshNeural Inhibition - Drug Effects - Physiologyen_US
dc.subject.meshNeurogenic Inflammation - Metabolism - Pathology - Therapyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Opioid, Kappa - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshReceptors, Opioid, Mu - Antagonists & Inhibitors - Physiologyen_US
dc.titleRostral ventromedial medulla μ, but not κ, opioid receptors are involved in electroacupuncture anti-hyperalgesia in an inflammatory pain rat modelen_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.brainres.2011.04.037en_US
dc.identifier.pmid21565329-
dc.identifier.scopuseid_2-s2.0-79957887450en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79957887450&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1395en_US
dc.identifier.spage38en_US
dc.identifier.epage45en_US
dc.identifier.isiWOS:000292426000005-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridZhang, Y=36045630100en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.scopusauthoridXin, J=23104505000en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US

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