dc.creatorPerin-Martins, A
dc.creatorTeixeira, JM
dc.creatorTambeli, CH
dc.creatorParada, CA
dc.creatorFischer, L
dc.date2013
dc.dateMAR
dc.date2014-07-30T13:40:55Z
dc.date2015-11-26T16:41:27Z
dc.date2014-07-30T13:40:55Z
dc.date2015-11-26T16:41:27Z
dc.date.accessioned2018-03-28T23:25:40Z
dc.date.available2018-03-28T23:25:40Z
dc.identifierJournal Of The Peripheral Nervous System. Wiley-blackwell, v. 18, n. 1, n. 62, n. 74, 2013.
dc.identifier1085-9489
dc.identifierWOS:000316696100011
dc.identifier10.1111/jns5.12010
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53535
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53535
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1272933
dc.descriptionThe aim of this study was to investigate the mechanisms that contribute to hyperalgesia and edema induced by TRPA1 activation. The injection of allyl isothiocyanate (AITC, 50, 100, or 300 mu g/paw) into the rat's hind paw induced dose and time-dependent hyperalgesia and edema, which were blocked by the selective TRPA1 antagonist, HC 030031 (1,200 mu g/paw), or by treatment with antisense oligodeoxynucleotide (four daily intrathecal injections of 5nmol). These results demonstrate that the hyperalgesia and edema induced by AITC depend on TRPA1 activation. AITC-induced hyperalgesia and edema were significantly reduced by treatment with neurokinin 1 (L-703,606, 38 mu g/paw) or calcitonin gene-related peptide (CGRP8-37, 5 mu g/paw) receptor antagonists, with a mast cell degranulator (compound 48/80, four daily injections of 1, 3, 10, and 10 mu g/paw) or with H1 (pyrilamine, 400 mu g/paw), 5-HT1A (wAy-100,135, 450 mu g/paw) or 5-HT3 (tropisetron, 450 mu g/paw) receptor antagonists. Pre-treatment with a selectin inhibitor (fucoidan, 20mg/kg) significantly reduced AITC-induced hyperalgesia, edema, and neutrophil migration. Finally, a cyclooxygenase inhibitor (indomethacin, 100 mu g/paw), a 1 (atenolol, 6 mu g/paw) or a 2 (ICI 118, 551, 1.5 mu g/paw) adrenoceptor antagonist also significantly reduced AITC-induced hyperalgesia and edema. Together, these results demonstrate that TRPA1 mediates some of the key inflammatory mechanisms, suggesting a key role of this receptor in pain and inflammation.
dc.description18
dc.description1
dc.description62
dc.description74
dc.languageen
dc.publisherWiley-blackwell
dc.publisherHoboken
dc.publisherEUA
dc.relationJournal Of The Peripheral Nervous System
dc.relationJ. Peripher. Nerv. Syst.
dc.rightsfechado
dc.rightshttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.sourceWeb of Science
dc.subjectedema
dc.subjecthyperalgesia
dc.subjectnociceptor sensitization
dc.subjectTRPA1
dc.subjectSubstance-p
dc.subjectNeurogenic Inflammation
dc.subjectCold Hyperalgesia
dc.subjectSensory Neurons
dc.subjectMast-cells
dc.subjectTrpa1
dc.subjectRat
dc.subjectActivation
dc.subjectPain
dc.subjectSensitization
dc.titleMechanisms underlying transient receptor potential ankyrin 1 (TRPA1)-mediated hyperalgesia and edema
dc.typeArtículos de revistas


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