dc.creatorTambeli, CH
dc.creatorLevine, JD
dc.creatorGear, RW
dc.date2009
dc.dateJUN
dc.date2014-11-19T16:47:15Z
dc.date2015-11-26T18:04:22Z
dc.date2014-11-19T16:47:15Z
dc.date2015-11-26T18:04:22Z
dc.date.accessioned2018-03-29T00:46:28Z
dc.date.available2018-03-29T00:46:28Z
dc.identifierPain. Elsevier Science Bv, v. 143, n. 3, n. 228, n. 232, 2009.
dc.identifier0304-3959
dc.identifierWOS:000266707900014
dc.identifier10.1016/j.pain.2009.03.005
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/62610
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/62610
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/62610
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1292829
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionThe duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR(5), mu-opioid, GABA(A), and GABA(B)), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABA(B) and mu-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR(5)), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the p-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors. (C) 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
dc.description143
dc.description3
dc.description228
dc.description232
dc.descriptionU.S. National Institutes of Health
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationPain
dc.relationPain
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectPain-induced analgesia
dc.subjectNucleus accumbens
dc.subjectSpinal cord
dc.subjectRat
dc.subjectAntinociception
dc.subjectCapsaicin
dc.subjectJaw-opening Reflex
dc.subjectVentrolateral Orbital Cortex
dc.subjectAnterior Pretectal Nucleus
dc.subjectPeriaqueductal Gray-matter
dc.subjectDorsal Horn
dc.subjectReceptor Antagonist
dc.subjectRat
dc.subjectAntinociception
dc.subjectNeurons
dc.subjectStimulation
dc.titleCentralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord
dc.typeArtículos de revistas


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