Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/30713
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dc.contributor.authorMarcotti, Aida-
dc.contributor.authorMiralles, Ana-
dc.contributor.authorDomínguez, Eduardo-
dc.contributor.authorPascual Gómez, Eliseo Ángel-
dc.contributor.authorGomis García, Ana María-
dc.contributor.authorBelmonte Martínez, Carlos-
dc.contributor.authorDe la Peña García, Elvira-
dc.contributor.otherDepartamentos de la UMH::Medicina Clínicaes_ES
dc.contributor.otherInstituto de Neurocienciases_ES
dc.contributor.otherDepartamentos de la UMH::Fisiologíaes_ES
dc.date.accessioned2024-01-26T10:27:04Z-
dc.date.available2024-01-26T10:27:04Z-
dc.date.created2018-04-
dc.identifier.citationPain 2018 Apr;159(4):739-748.es_ES
dc.identifier.issn1872-6623 (Electronic)-
dc.identifier.urihttps://hdl.handle.net/11000/30713-
dc.description.abstractThe mechanisms whereby deposition of monosodium urate (MSU) crystals in gout activates nociceptors to induce joint pain are incompletely understood. We tried to reproduce the signs of painful gouty arthritis, injecting into the knee joint of rats suspensions containing amorphous or triclinic, needle MSU crystals. The magnitude of MSU-induced inflammation and pain behavior signs were correlated with the changes in firing frequency of spontaneous and movement-evoked nerve impulse activity recorded in single knee joint nociceptor saphenous nerve fibers. Joint swelling, mechanical and cold allodynia, and hyperalgesia appeared 3 hours after joint injection of MSU crystals. In parallel, spontaneous and movement-evoked joint nociceptor impulse activity raised significantly. Solutions containing amorphous or needle-shaped MSU crystals had similar inflammatory and electrophysiological effects. Intraarticular injection of hyaluronan (HA, Synvisc), a high-MW glycosaminoglycan present in the synovial fluid with analgesic effects in osteoarthritis, significantly reduced MSU-induced behavioral signs of pain and decreased the enhanced joint nociceptor activity. Our results support the interpretation that pain and nociceptor activation are not triggered by direct mechanical stimulation of nociceptors by MSU crystals, but are primarily caused by the release of excitatory mediators by inflammatory cells activated by MSU crystals. Intra-articular HA decreased behavioral and electrophysiological signs of pain, possibly through its viscoelastic filtering effect on the mechanical forces acting over sensitized joint sensory endings and probably also by a direct interaction of HA molecules with the transducing channels expressed in joint nociceptor terminals.es_ES
dc.formatapplication/pdfes_ES
dc.format.extent10es_ES
dc.language.isoenges_ES
dc.publisherLippincott, Williams & Wilkins [Commercial Publisher]es_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectGoutes_ES
dc.subjectArthritises_ES
dc.subjectHyaluronanes_ES
dc.subjectNociceptorses_ES
dc.subjectKnee-joint inflammationes_ES
dc.subjectTRP channelses_ES
dc.titleJoint nociceptor nerve activity and pain in an animal model of acute gout and its modulation by intra-articular hyaluronanes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversion10.1097/j.pain.0000000000001137es_ES
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