首页> 外文期刊>Behavioural Brain Research: An International Journal >Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: comparison of reserpine-induced myalgia and chronic constriction injury rats.
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Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: comparison of reserpine-induced myalgia and chronic constriction injury rats.

机译:纤维肌痛和神经性疼痛的不同病理生理基础动物模型:利血平诱发的肌痛和慢性收缩损伤大鼠的比较。

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The reserpine-induced myalgia (RIM) rat manifests fibromyalgia-like chronic pain symptoms. The present study explored the pathophysiology underlying the pain symptoms in the RIM rat and the chronic constriction injury (CCI) rat, an animal model of neuropathic pain as a reference. Nerve tissue samples were collected from the nociception-tested animals for pathological examinations. Additionally, the therapeutic efficacy of a sodium channel blocker mexiletine was assessed in both rats. A slight vacuolization in the substantia nigra (SN) occurred in some of the RIM rats without any other histopathological changes in the brain or peripheral neurons. All the RIM rats, with or without vacuolization, showed hypersensitivity to tactile, muscle pressure, and cold stimuli. In the CCI rat, neurodegenerative changes were apparent in the sciatic nerve and the spinal cord only. CCI rats displayed muscle hyperalgesia in addition to tactile and cold allodynia. Pharmacotherapy with mexiletine did not attenuate the pain in the RIM rat, although it was effective in the CCI rat. Taken together, it is not likely that pain symptoms in RIM rats are caused by degenerative changes at the level of primary afferents and spinal cord, as is the case for CCI rats. The significance of the vacuolization in the SN is less clear at present because of the minor extent of the change and the lack of correlation with nociceptive sensitivity. The pain symptoms in RIM rats could be associated with dysfunction of biogenic amines-mediated CNS pain control even without apparent pathologies in the nervous system.
机译:利血平诱发的肌痛(RIM)大鼠表现出纤维肌痛样慢性疼痛症状。本研究探讨了RIM大鼠和慢性收缩性损伤(CCI)大鼠疼痛症状的病理生理学,该动物是神经性疼痛的动物模型,以作为参考。从经过伤害感受测试的动物中收集神经组织样本,以进行病理检查。另外,在两只大鼠中评估了钠通道阻滞剂美西律的治疗功效。在一些RIM大鼠中,黑质(SN)发生了轻微的空泡,而大脑或周围神经元没有任何其他组织病理学改变。所有有或没有空泡的RIM大鼠均表现出对触觉,肌肉压力和冷刺激的超敏反应。在CCI大鼠中,仅在坐骨神经和脊髓中神经退行性改变是明显的。 CCI大鼠除了触觉和冷异常性疼痛外,还表现出肌肉痛觉过敏。尽管美西律汀在CCI大鼠中有效,但其药物治疗并未减轻RIM大鼠的疼痛。综上所述,RIM大鼠的疼痛症状不太可能像CCI大鼠那样是由初级传入和脊髓水平的退行性变化引起的。目前,SN中空泡化的意义尚不十分清楚,这是因为变化程度较小,并且与伤害感受性敏感性缺乏相关性。 RIM大鼠的疼痛症状可能与生物胺介导的CNS疼痛控制功能障碍有关,即使在神经系统中没有明显的病理情况。

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