Activation of Erk in the anterior cingulate cortex during the induction and expression of chronic pain.
Activation of Erk in the anterior cingulate cortex during the induction and expression of chronic pain.
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DOI：
10.1186/1744-8069-4-28
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发表时间：
2008-07-23
期刊：
影响因子：
3.3
通讯作者：
Zhuo M
中科院分区：
文献类型：
--
作者：
Wei F;Zhuo M
细胞外信号调节激酶（Erk）活性有助于突触可塑性，这是学习、记忆和慢性疼痛的关键机制。虽然前扣带皮层（ACC）已被报道为一个重要的皮质区域的神经元机制的诱导和表达的慢性疼痛，它尚未被调查是否在ACC的ERK活性可能受到外周损伤或慢性疼痛状态。在本研究中，我们使用成年大鼠动物模型的炎症性和神经病理性疼痛，并证明，在ACC的ERK信号通路是有力的激活后，外周组织或神经损伤。此外，我们证明，机械异常性疼痛显着激活ERK活性在突触部位损伤后两周。我们提出了一个突触模型来解释Erk活性在慢性疼痛不同阶段的作用。我们的研究结果表明，皮层激活的ERK可能有助于诱导和表达慢性疼痛。
The extracellular signal-regulated kinase (Erk) activity contributes to synaptic plasticity, a key mechanism for learning, memory and chronic pain. Although the anterior cingulate cortex (ACC) has been reported as an important cortical region for neuronal mechanisms underlying the induction and expression of chronic pain, it has yet to be investigated whether or not Erk activity in the ACC may be affected by peripheral injury or in chronic pain state. In the present study, we use adult rat animal models of inflammatory and neuropathic pain and demonstrate that Erk signaling pathway in the ACC is potently activated after peripheral tissue or nerve injury. Furthermore, we demonstrate that mechanical allodynia significantly activated Erk activity at synaptic sites at two weeks after the injury. We propose a synaptic model for explaining the roles of Erk activity during different phases of chronic pain. Our findings suggest that cortical activation of Erk may contribute to both induction and expression of chronic pain.
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影响因子：
25
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