Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other pathological signs remain unresolved. We have previously reported that inflammatory signs, contractures, disuse muscle atrophy, spontaneous pain-like behaviors, and chronic widespread mechanical hyperalgesia based on central plasticity occurred after 2 weeks of cast immobilization in chronic post-cast pain (CPCP) rat model. In this study, we also demonstrated dystrophy-like changes, both peripheral nociceptive signals and activation of the central pain pathway in CPCP rats. This was done by the following methods: (1) vascular permeability (Evans blue dye) and inflammatory- and oxidative stress-related messenger RNA changes (real-time quantitative polymerase chain reaction); (2) immunofluorescence of pERK and/or c-Fos expression in the spino-parabrachio-amygdaloid pathway; and (3) blockade of nociceptive-related signals using sciatic nerve block. Furthermore, we demonstrated tactile allodynia using an optogenetic method in a transgenic rat line (W-TChR2V4), cold allodynia using the acetone test, and activation of dorsal horn neurons in the chronic phase associated with chronic mechanical hyperalgesia using c-Fos immunofluorescence. In addition, we showed that nociceptive signals in the acute phase are involved in chronic pathological pain-like behaviors by studying the effects of sciatic nerve block. Thus, we conclude that physical disuse contributes to dystrophy-like changes, spontaneous pain-like behavior, and chronic widespread pathological pain-like behaviors in CPCP rats after 2 weeks of cast immobilization.

译文

由于害怕通过运动 (运动恐惧症) 或不适当的休息程序而引起的疼痛,身体上的不使用可能导致以I型复杂区域疼痛综合征为代表的慢性疼痛状态。然而,身体使用与急/慢性疼痛和其他病理体征相关的机制仍未解决。我们以前曾报道,在慢性铸后疼痛 (CPCP) 大鼠模型中,在石膏固定2周后发生了炎症体征,挛缩,废用肌肉萎缩,自发性疼痛样行为和基于中枢可塑性的慢性广泛的机械痛觉过敏。在这项研究中,我们还证明了CPCP大鼠的营养不良样变化,包括外周伤害感受信号和中枢疼痛途径的激活。这是通过以下方法完成的 :( 1) 血管通透性 (伊文思蓝染料) 和炎症和氧化应激相关的信使RNA变化 (实时定量聚合酶链反应); (2) spino-parabrachio-杏仁核途径中pERK和/或c-Fos表达的免疫荧光; (3) 使用坐骨神经阻滞阻断伤害性相关信号。此外,我们在转基因大鼠品系 (W-TChR2V4) 中使用光遗传学方法证明了触觉异常性疼痛,使用丙酮测试证明了冷异常性疼痛,以及使用c-Fos免疫荧光激活与慢性机械痛觉过敏相关的慢性期背角神经元。此外,通过研究坐骨神经阻滞的作用,我们发现急性期的伤害性信号与慢性病理性疼痛样行为有关。因此,我们得出的结论是,石膏固定2周后,CPCP大鼠的身体使用会导致营养不良样变化,自发性疼痛样行为和慢性广泛的病理性疼痛样行为。

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