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GAZZETTA MEDICA ITALIANA ARCHIVIO PER LE SCIENZE MEDICHE

A Journal on Internal Medicine and Pharmacology


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Gazzetta Medica Italiana Archivio per le Scienze Mediche 2014 March;173(3):127-34

Copyright © 2014 EDIZIONI MINERVA MEDICA

language: English

Role of voltage-dependent sodium channel subtype 1.7 (Nav 1.7) in pathophysiology of fibromyalgia

De Freitas Brito A. 1, 2, Silva A. S. 1, Souto Pereira C. K. 1, 3, Araújo Silva B. 1, 2, 4

1 Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos do Centro de Ciências da Saúde, da Universidade Federal da Paraíba (UFPB); 2 Laboratório de Farmacologia Funcional, Prof. George Thomas do Centro de Ciências da Saúde da Universidade federal da Paraíba (UFPB); 3 Laboratório de Psicofarmacologia Prof. Elizaldo A. Carlini do Centro de Ciências da Saúde da Universidade Federal da Paraíba (UFPB); 4 Departamento de Ciências Farmacêuticas do Centro de Ciências da Saúde da Universidade Federal da Paraíba (UFPB)


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Fibromyalgia (FM) is a neuropathic pain syndrome that does not affect the joints, characterized by chronic diffuse musculoskeletal pain, being the most common cause of widespread pain of the general population. Investigations suggest that autonomic dysfunction, maintained by sympathetic activity, may explain the characteristics of FM that is a neuropathic pain syndrome. Dorsal root ganglia (DRG) are potential sites with sympathetic-nociceptive interaction. Sodium channels located in dorsal root ganglia, specifically the voltage-dependent sodium channels subtype 1.7 (Nav 1.7) act as a molecular gatekeepers controllers of the peripheral nociceptors on the detection of the pain. Trauma or infection can induce neuroplasticity with an overexpression of sympathetic fibers and sodium channels in dorsal root ganglia, so that the nerve growth factor mediates these phenotypic changes enabling catecholamines and/or sympathetic impulses to activate nociceptors. It has been proposed that enhanced GRD excitability may play a role in fibromyalgia pain. Individuals with FM are those genetically determined sympathetic hyperactivity, or those with inherent channelopathies Nav. In view of the foregoing, we will elucidate in this review, that the participation of Nav 1.7 in the genesis of FM, and possible selective channel blockers for this subtype, as a future therapeutic option for this disease.

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