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首页> 外文期刊>Pain. >The ontogeny of neuropathic pain: postnatal onset of mechanical allodynia in rat spared nerve injury (SNI) and chronic constriction injury (CCI) models.
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The ontogeny of neuropathic pain: postnatal onset of mechanical allodynia in rat spared nerve injury (SNI) and chronic constriction injury (CCI) models.

机译:神经性疼痛的个体发生:大鼠幸存的神经损伤(SNI)和慢性压迫损伤(CCI)模型中机械性异常性疼痛的产后发作。

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摘要

Neuropathic pain is known to occur in children but remains poorly understood and treated. The aim here was to establish a model of neuropathic pain in neonatal and young rodents. In the adult the spared nerve injury (SNI) model produced robust mechanical allodynia measured as a fall in cutaneous sensory threshold to 16% of controls, within one postoperative day and lasting at least 28 days. In contrast, animals aged 3, 10 and 21 days at the time of surgery did not display equivalent allodynia at any time up to 28 days later. A small, transient bilateral increased cutaneous sensitivity was observed at day 7 in P10 and P21 animals but this had gone by 14 days. SNI performed at 33 days led to a significant and persistent allodynia with the threshold falling to 55% of control values. A similar lack of neuropathic pain behaviour in younger animals was observed using the chronic constriction injury (CCI) model, which produced a clear allodynia in adult rats but no change in hindpaw sensitivity when performedat 10 days of age. Mechanical allodynia can be evoked in very young animals with inflammatory pain, so this developmental profile is selective for peripheral neuropathic pain and suggests a remarkable ability in young animals to compensate for the sensory consequences of nerve injury. The results are consistent with human neonatal responses to nerve injury; further study of underlying mechanisms are likely to yield important information about the pathogenesis and treatment of neuropathic pain.
机译:已知神经性疼痛会发生在儿童中,但人们对其了解和治疗仍知之甚少。这里的目的是建立新生和年轻啮齿动物的神经性疼痛模型。在成年人中,幸存的神经损伤(SNI)模型在术后一天之内且持续至少28天,产生了强大的机械异常性疼痛,其测量为皮肤感觉阈值下降至对照组的16%。相反,在手术时第3、10和21天的动物直到28天后的任何时候都没有表现出同等的异常性疼痛。在P10和P21动物中,在第7天观察到短暂的,短暂的双侧皮肤敏感性增加,但是已经过去了14天。在第33天进行的SNI导致明显的持续性异常性疼痛,其阈值降至对照值的55%。使用慢性收缩损伤(CCI)模型可观察到在幼小动物中类似的神经性疼痛行为缺乏,该模型在成年大鼠中产生明显的异常性疼痛,但在10天龄时后爪敏感性没有变化。机械性异常性疼痛可以在非常年轻的患有炎性疼痛的动物中诱发,因此这种发育状况对周围神经性疼痛具有选择性,并表明年幼动物具有显着的能力来补偿神经损伤的感觉后果。结果与人类新生儿对神经损伤的反应一致;对潜在机制的进一步研究可能会提供有关神经性疼痛的发病机理和治疗的重要信息。

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