Activation of the Extracellular Signal-Regulated Kinase in the Amygdale Modulates Fentanyl-Induced Hypersensitivity in Rats

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• 作者：Zhen Li^&lowast ; ; ^&dagger ; ; Pingping Yin^&lowast ; ; ^&dagger ; ; Jian Chen^&lowast ; ; Chenhong Li^&lowast ; ; Jieqiong Liu^&dagger ; ; Hemanshu Rambojan^&dagger ; ; Fang Luo^&dagger ; ; ^{luofang0909@hotmail.com}
• 关键词：Pain ; opioid-induced hyperalgesia ; extracellular signal-regulated MAP kinases ; central amygdaloid nucleus ; central nervous system sensitization ; long-term potentiation
• 刊名：The Journal of Pain
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：18
• 期：2
• 页码：188-199
• 全文大小：1709 K
• 卷排序：18

文摘

The level of phospho-extracellular signal-regulated kinase in the right laterocapsular division of the central nucleus of amygdale (CeLC) was increased in the fentanyl-induced hypersensitivity rats. Microinjection of U0126, an extracellular signal-regulated kinase inhibitor, into the CeLC reversed the mechanical and thermal hypersensitivity induced by fentanyl in a dose-dependent manner. Synaptic transmission in CeLC neurons was increased in fentanyl-induced hypersensitivity rats, which also could be abolished by U0126. In vivo microinjection of U0126 into the CeLC reversed the spinal long-term potentiation in opioid-induced hyperalgesia rats.