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Physical exercise is a common treatment for low back pain. The possible mechanisms underlying the effects of exercise are probably multifold. This work shows that swimming exercise prevents sensitization of dorsal horn neurons, which may be one mechanism for the positive effects of exercise.

This study aimed to evaluate whether the development and/or maintenance of chronic-latent muscle hyperalgesia is modulated by P2X3 receptors. We also evaluate the expression of P2X3 receptors and PKCε of dorsal root ganglions during these processes. A mouse model of chronic-latent muscle hyperalgesia, induced by carrageenan and evidenced by PGE 2 , was used. Mechanical muscle hyperalgesia was measured by Randall-Selitto analgesimeter. The involvement of P2X3 receptors was analyzed by using the selective P2X3 receptors antagonist A-317491 by intramuscular or intrathecal injections. Expression of P2X3 and PKCε in dorsal root ganglion (L4-S1) were evaluated by Western blotting. Intrathecal blockade of P2X3 receptors previously to carrageenan prevented the development and maintenance of acute and chronic-latent muscle hyperalgesia, while intramuscular blockade of P2X3 receptors previously to carrageenan only reduced the acute muscle hyperalgesia and had no effect on chronic-latent muscle hyperalgesia. Intrathecal, but not intramuscular, blockade of P2X3 receptors immediately before PGE 2 , in animals previously sensitized by carrageenan, reversed the chronic-latent muscle hyperalgesia. There was an increase in total and phosphorylated PKCε 48 h after the beginning of acute muscle hyperalgesia, and in P2X3 receptors at the period of chronic muscle hyperalgesia. P2X3 receptors expressed on spinal cord dorsal horn contribute to transition from acute to chronic muscle pain. We also suggest an interaction of PKCε and P2X3 receptors in this process. Therefore, we point out P2X3 receptors of the spinal cord dorsal horn as a pharmacological target to prevent the development or reverse the chronic muscle pain conditions.

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ResumoOs receptores PPARγ (Receptores Ativados por Proliferadores de Peroxissoma Gama) emergiram como um alvo promissor para o tratamento de processos dolorosos, uma vez que os seus agonistas suprimem a dor inflamatória. Sabe-se que o exercício tambem é um tratamento eficaz para dores musculares e que um dos mecanismos pelo qual isso ocorre é através da ativação dos receptores PPARγ. No entanto seu mecanismo de ação não está completamente elucidado. Sendo assim, o objetivo desse estudo foi analisar se os receptores PPARγ modulam a hipoalgesia induzida pelo exercicio físico através da inibição da liberação local de TNF-α ou CINC-1. Palavras-chave:Hiperalgesia, CINC-1, exercício crônico

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