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dc.contributor.authorNieto López, Francisco Rafael 
dc.contributor.authorCendán Martínez, Cruz Miguel 
dc.contributor.authorCañizares, Francisco J.
dc.contributor.authorCubero Sánchez, María Angustias
dc.contributor.authorVela, José M.
dc.contributor.authorFernández Segura, Eduardo 
dc.contributor.authorBaeyens Cabrera, José Manuel 
dc.date.accessioned2014-03-11T13:07:01Z
dc.date.available2014-03-11T13:07:01Z
dc.date.issued2014
dc.identifier.citationNieto, F.R.; et al. Genetic inactivation and pharmacological blockade of sigma-1 receptors prevent paclitaxel-induced sensory-nerve mitochondrial abnormalities and neuropathic pain in mice. Molecular Pain, 10: 11 (2014). [http://hdl.handle.net/10481/30783]es_ES
dc.identifier.issn1744-8069
dc.identifier.otherdoi: 10.1186/1744-8069-10-11
dc.identifier.urihttp://hdl.handle.net/10481/30783
dc.description.abstractBackground Paclitaxel, a widely-used antineoplastic drug, produces a painful peripheral neuropathy that in rodents is associated with peripheral-nerve mitochondrial alterations. The sigma-1 receptor (σ1R) is a ligand-regulated molecular chaperone involved in mitochondrial calcium homeostasis and pain hypersensitivity. This receptor plays a key role in paclitaxel-induced neuropathic pain, but it is not known whether it also modulates mitochondrial abnormalities. In this study, we used a mouse model of paclitaxel-induced neuropathic pain to test the involvement of the σ1R in the mitochondrial abnormalities associated with paclitaxel, by using genetic (σ1R knockout mice) and pharmacological (σ1R antagonist) approaches.es_ES
dc.description.abstractResults Paclitaxel administration to wild-type (WT) mice produced cold- and mechanical-allodynia, and an increase in the frequency of swollen and vacuolated mitochondria in myelinated A-fibers, but not in C-fibers, of the saphenous nerve. Behavioral and mitochondrial alterations were marked at 10 days after paclitaxel-administration and had resolved at day 28. In contrast, paclitaxel treatment did not induce allodynia or mitochondrial abnormalities in σ1R knockout mice. Moreover, the prophylactic treatment of WT mice with BD-1063 also prevented the neuropathic pain and mitochondrial abnormalities induced by paclitaxel.es_ES
dc.description.abstractConclusions These results suggest that activation of the σ1R is necessary for development of the sensory nerve mitochondrial damage and neuropathic pain produced by paclitaxel. Therefore, σ1R antagonists might have therapeutic value for the prevention of paclitaxel-induced neuropathy.es_ES
dc.description.sponsorshipThis study was partially supported by grant P11-CTS-7649 and grant CTS-109 from Junta de Andalucía, FEDER funds, a grant from Esteve, and a grant from the Centro para el Desarrollo Tecnológico Industrial (NeoGenius Pharma project). F. R. Nieto was supported by a FPU grant from the Spanish Ministerio de Educación y Ciencia (MEC) and C. M. Cendán by the Research Program of the University of Granada.es_ES
dc.language.isoenges_ES
dc.publisherBiomed Centrales_ES
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs 3.0 License
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subjectPaclitaxeles_ES
dc.subjectSigma-1 receptorses_ES
dc.subjectChemotherapy-induced peripheral neuropathyes_ES
dc.subjectBD-1063es_ES
dc.subjectMitochondriaes_ES
dc.subjectAllodyniaes_ES
dc.subjectNeuropathic paines_ES
dc.subjectSigma-1 receptor knockout micees_ES
dc.titleGenetic inactivation and pharmacological blockade of sigma-1 receptors prevent paclitaxel-induced sensory-nerve mitochondrial abnormalities and neuropathic pain in micees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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