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Endogenous interleukin-6 contributes to hypersensitivity to cutaneous stimuli and changes in neuropeptides associated with chronic nerve constriction in mice.
Murphy, P G; Ramer, M S; Borthwick, L; Gauldie, J; Richardson, P M; Bisby, M A.
Afiliación
  • Murphy PG; Department of Physiology, Queen's University, Kingston, Canda K7L 3N63.
Eur J Neurosci ; 11(7): 2243-53, 1999 Jul.
Article en En | MEDLINE | ID: mdl-10383613
Partial nerve injury is a potential cause of distressing chronic pain for which conventional analgesic treatment with opiates or anti-inflammatory agents is not very effective. Constriction nerve injury, widely used to study neuropathic pain, was shown here to induce interleukin-6 (IL-6) mRNA in a subset of rat primary sensory neurons. When we inflicted chronic nerve constriction on mice with null mutation of the IL-6 gene, the hypersensitivity to cutaneous heat and pressure that is induced in wild-type mice was not evident, the loss of substance P in sensory neurons was excessive and the induction of galanin in central sensory projections was reduced. In additional experiments, intrathecal infusion of IL-6 in rats was shown to stimulate synthesis of galanin in approximately one-third of lumbar dorsal root ganglion neurons. The results of these experiments indicate that endogenous IL-6 mediates some of the hypersensitive responses that characterize peripheral neuropathic pain, and influences two neuropeptides that have been implicated in pain transmission.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piel / Neuropéptidos / Interleucina-6 / Hiperestesia / Síndromes de Compresión Nerviosa Tipo de estudio: Etiology_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Eur J Neurosci Asunto de la revista: NEUROLOGIA Año: 1999 Tipo del documento: Article Pais de publicación: Francia
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piel / Neuropéptidos / Interleucina-6 / Hiperestesia / Síndromes de Compresión Nerviosa Tipo de estudio: Etiology_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Eur J Neurosci Asunto de la revista: NEUROLOGIA Año: 1999 Tipo del documento: Article Pais de publicación: Francia