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首页> 外文期刊>The European Journal of Neuroscience >Primary afferent nociceptor mechanisms mediating NGF-induced mechanical hyperalgesia.
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Primary afferent nociceptor mechanisms mediating NGF-induced mechanical hyperalgesia.

机译：初级传入伤害感受器机制介导NGF诱导的机械痛觉过敏。

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摘要

The underlying mechanism for nerve growth factor (NGF) evoked pain and long-lasting mechanical hyperalgesia remains poorly understood. Using intrathecal antisense against the NGF receptor, receptor tyrosine kinase (TrkA), we found NGF to act at the primary afferent nociceptor directly in the Sprague-Dawley rat. Inhibitors of the three major pathways for TrkA receptor signalling, extracellular signal-related kinase (ERK)/mitogen-activated protein kinase kinase (MEK) (ERK/MEK), phosphatidylinositol 3-kinase (PI3K), and phospholipase Cgamma (PLCgamma) all attenuate NGF-induced hyperalgesia. Although inhibitors of kinases downstream of PI3K and PLCgamma[glycogen synthetase kinase 3 (GSK3), calmodulin-dependent protein kinase II (CAMII-K) or protein kinase C (PKC)] do not reduce mechanical hyperalgesia, hyperalgesia induced by activation of PI3K was blocked by ERK/MEK inhibitors, suggesting cross-talk from the PI3K to the ERK/MEK signalling pathway. As integrins have been shown to modulate epinephrine and prostaglandin E(2)-induced hyperalgesia, we also evaluated a role for integrins in NGF-induced mechanical hyperalgesia using beta(1)-integrin-specific antisense or antibodies.
机译：对于神经生长因子（NGF）引起的疼痛和持久的机械性痛觉过敏的潜在机制仍然知之甚少。使用针对NGF受体鞘氨醇酪氨酸激酶（TrkA）的鞘内反义，我们发现NGF直接作用于Sprague-Dawley大鼠的主要传入伤害感受器。 TrkA受体信号传导，细胞外信号相关激酶（ERK）/丝裂原活化蛋白激酶激酶（MEK）（ERK / MEK），磷脂酰肌醇3-激酶（PI3K）和磷脂酶Camma（PLCgamma）的三种主要途径的抑制剂减轻NGF引起的痛觉过敏。尽管PI3K和PLCgamma [糖原合成酶激酶3（GSK3），钙调蛋白依赖性蛋白激酶II（CAMII-K）或蛋白激酶C（PKC）]下游激酶的抑制剂不能减少机械性痛觉过敏，但由PI3K激活引起的痛觉过敏却是被ERK / MEK抑制剂阻断，表明从PI3K到ERK / MEK信号通路的串扰。由于整合素已显示出调节肾上腺素和前列腺素E（2）诱导的痛觉过敏，我们还评估了整合素在NGF诱导的机械性痛觉过敏中的作用，使用β（1）-整合素特异性反义或抗体。

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