Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity
Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity
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DOI：
10.1038/16040
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发表时间：
1999-12-01
影响因子：
25
通讯作者：
Woolf, CJ
中科院分区：
文献类型：
--
作者：
Ji, RR;Baba, H;Woolf, CJ
我们研究了脊髓神经元内细胞外信号调节蛋白激酶（ERK）在产生疼痛超敏反应中的作用。在一分钟内的一个强烈的有害的周边或C-纤维电刺激，许多磷酸化ERK阳性神经元观察到，最主要的是在板层I和IIo的同侧背角。这种染色是强度和NMDA受体依赖性的。低强度刺激或A纤维输入没有影响。MEK抑制剂抑制ERK磷酸化可减少福尔马林诱导的疼痛行为的第二阶段，这是脊髓神经元致敏的一种衡量标准。因此，脊髓内的ERK信号传导参与产生疼痛超敏性。由于其快速激活，这种效应可能涉及调节神经元兴奋性而不改变转录。
We investigated the involvement of extracellular signal-regulated protein kinases (ERK) within spinal neurons in producing pain hypersensitivity. Within a minute of an intense noxious peripheral or C-fiber electrical stimulus, many phosphoERK-positive neurons were observed, most predominantly in lamina I and IIo of the ipsilateral dorsal horn. This staining was intensity and NMDA receptor dependent. Low-intensity stimuli or A-fiber input had no effect. Inhibition of ERK phosphorylation by a MEK inhibitor reduced the second phase of formalin-induced pain behavior, a measure of spinal neuron sensitization. ERK signaling within the spinal cord is therefore involved in generating pain hypersensitivity. Because of its rapid activation, this effect probably involves regulation of neuronal excitability without changes in transcription.