Spinal mechanisms of neuropathic pain: Is there a P2X4-BDNF controversy?
Spinal mechanisms of neuropathic pain: Is there a P2X4-BDNF controversy?
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DOI：
10.1016/j.ynpai.2017.04.001
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发表时间：
2017-01-01
期刊：
影响因子：
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通讯作者：
Malcangio, Marzia
中科院分区：
文献类型：
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作者：
Malcangio, Marzia
十多年前，神经胶质细胞是脊髓疼痛机制调节的主要参与者的新概念已经开始了一系列多产的工作，解决了神经元-神经胶质细胞通信的方式。Mike Salter与Kazuhide Inoue实验室通过激活周围神经损伤同侧背角中小胶质细胞表达的P2 X4受体，将ATP作为这种通信的关键介质。P2 X4受体的激活导致神经营养因子BDNF的释放，其通过神经元TrkB受体的激活改变神经元兴奋性，并且该效应与行为同侧异常性疼痛相关。这篇观点文章比较了支持P2 X4和BDNF系统在神经性疼痛中的生物学相关性的证据与最近质疑这种重要性的数据。读了这篇文章后，读者将能够对这种争议提出自己的看法。
More than a decade ago the novel concept that glial cells are major players in the modulation of pain mechanisms in the spinal cord has started a prolific series of work addressing the modalities of neuron-glia communication. Mike Salter with Kazuhide Inoue laboratories introduced ATP as pivotal mediator for such communication via activation of P2X4 receptors expressed by microglia in the dorsal horn ipsilateral to a peripheral nerve injury. Activation of P2X4 receptors result in release of the neurotrophin BDNF, which, through the activation of neuronal TrkB receptors, alters neuronal excitability and this effect is associated with behavioural ipsilateral allodynia. This viewpoint article compares the evidence supporting a biological relevance of the P2X4 and BDNF system in neuropathic pain with recent data which question such importance. Having read this article, readers will be able to formulate their own opinion on such controversy.