Ankle joint mobilization reduces axonotmesis-induced neuropathic pain and glial activation in the spinal cord and enhances nerve regeneration in rats |
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Authors: | Martins Daniel F Mazzardo-Martins Leidiane Gadotti Vinícius M Nascimento Francisney P Lima Denise A N Speckhann Breno Favretto Gisela A Bobinski Franciane Cargnin-Ferreira Eduardo Bressan Elisângela Dutra Rafael C Calixto João B Santos Adair R S |
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Affiliation: | aLaboratório de Neurobiologia da Dor e Inflamação, Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Florianópolis, SC, Brazil;bPrograma de Pós-graduação em Neurociências, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Florianópolis, SC, Brazil;cLaboratório de Marcadores Histológicos, Instituto Federal de Educação, Ciência e Tecnologia de Santa Catarina, Campus Lages, Lages, SC, Brazil;dDepartamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Florianópolis, SC, Brazil |
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Abstract: | An important issue in physical rehabilitation is how to protect from or to reduce the effects of peripheral nerve injury. In the present study, we examined whether ankle joint mobilization (AJM) would reduce neuropathic pain and enhance motor functional recovery after nerve injury. In the axonotmesis model, AJM during 15 sessions every other day was conducted in rats. Mechanical and thermal hyperalgesia and motor performance deficit were measured for 5 weeks. After 5 weeks, we performed morphological analysis and quantified the immunoreactivity for CD11b/c and glial fibrillary acidic protein (GFAP), markers of glial activation, in the lumbar spinal cord. Mechanical and thermal hyperalgesia and motor performance deficit were found in the Crush + Anesthesia (Anes) group (P < 0.001), which was significantly decreased after AJM (P < 0.001). In the morphological analysis, the Crush + Anes group presented reduced myelin sheath thickness (P < 0.05), but the AJM group presented enhanced myelin sheath thickness (P < 0.05). Peripheral nerve injury increased the immunoreactivity for CD11b/c and GFAP in the spinal cord (P < 0.05), and AJM markedly reduced CD11b/c and GFAP immunoreactivity (P < 0.01). These results show that AJM in rats produces an antihyperalgesic effect and peripheral nerve regeneration through the inhibition of glial activation in the dorsal horn of the spinal cord. These findings suggest new approaches for physical rehabilitation to protect from or reduce the effects of nerve injury. |
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Keywords: | Joint mobilization Neuropathic pain Spinal cord Microglia Astrocytes |
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