Exercise therapy normalizes BDNF upregulation and glial hyperactivity in a mouse model of neuropathic pain

Autor(es)

Almeida, Cayo ^[1] ; DeMaman, Aline ^[1] ; Kusuda, Ricardo ^[1] ; Cadetti, Flaviane ^[1] ; Ravanelli, Maria Ida ^[1] ; Queiroz, Andre L. ^[2] ; Sousa, Thais A. ^[3] ; Zanon, Sonia ^[1] ; Silveira, Leonardo R. ^[4] ; Lucas, Guilherme ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Physiol, Lab Pain Neurobiol, BR-05508 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Biochem & Immunol, BR-05508 Sao Paulo - Brazil

^[3] Fed Inst Educ Sci & Technol Goias, Goiania, Go - Brazil

^[4] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, BR-05508 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Pain; v. 156, n. 3, p. 504-513, MAR 2015.
• Citações Web of Science: 41

Resumo

Treatment of neuropathic pain is a clinical challenge likely because of the time-dependent changes in many neurotransmitter systems, growth factors, ionic channels, membrane receptors, transcription factors, and recruitment of different Cell types. Conversely, an increasing number of reports have shown the ability of extended and regular physical exercise in alleviating neuropathic pain throughout a wide range of Mechanisms. In this study, we investigate the effect of swim exercise on molecules associated with initiation and maintenance of nerve injury-induced neuropathic pain. BALB/c mice were submitted to partial ligation of the sciatic nerve followed by a 5-week aerobbic exercise program. Physical training reversed mechanical hypersensitivity, which lasted for an additional 4 weeks after exercise interruption. Swim exercise normalized nerve injury-induced nerve growth factor, and brain-derived neurotrophic factor (BDNF) enhanced expression in the dorsal root ganglion, but had no effect on the glial-derived neurotrophic factor. However, only BDNF remained at low levels after exercise interruption. In addition, exercise training significantly reduced the phosphorylation status of PLC gamma-1, but not CREB, in the spinal cord dorsal horn in response to nerve injury. Finally, prolonged swim exercise reversed astrocyte and microglia hyperactivity in the dorsal horn after nerve lesion, which remained normalized after training cessation. Together, these results demonstrate that exercise therapy induces long-lasting analgesia through various mechanisms associated with the onset and advanced stages of neuropathy. Moreover, the data support further studies to clarify whether appropriate exercise intensity, volume, and duration can also cause long-lasting,pain relief in with neuropathic pain: (AU)

• Processo FAPESP: 11/08364-6 - Ação do exercício sobre a expressão e atividade de ligantes da família do Fator Neurotrófico Derivado da Glia: integrando mecanismos de dor neuropática e o valor terapêutico da atividade física.
• Beneficiário: Aline dos Santos de Maman
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 09/16926-4 - Ação do exercício sobre a expressão e atividade de ligantes da família do fator neurotrófico derivado da glia: integrando mecanismos de dor neuropática e o valor terapêutico da atividade física
• Beneficiário: Guilherme de Araújo Lucas
• Modalidade de apoio: Auxílio à Pesquisa - Regular