Title |
Genetic Inactivation and Pharmacological Blockade of Sigma-1 Receptors Prevent Paclitaxel-Induced Sensory-Nerve Mitochondrial Abnormalities and Neuropathic Pain in Mice
|
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Published in |
Molecular Pain, January 2014
|
DOI | 10.1186/1744-8069-10-11 |
Pubmed ID | |
Authors |
Francisco R Nieto, Cruz M Cendán, Francisco J Cañizares, María A Cubero, José M Vela, Eduardo Fernández-Segura, José M Baeyens |
Abstract |
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. |
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