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首页> 外文期刊>The European Journal of Neuroscience >Evidence for a role of CaMKIV in the development of opioid analgesic tolerance.
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Evidence for a role of CaMKIV in the development of opioid analgesic tolerance.

机译：CaMKIV在类阿片镇痛耐受性发展中的作用的证据。

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摘要

cAMP response-element binding protein (CREB), a transcription factor involved in learning, memory and drug addiction, is phosphorylated by calcium-calmodulin-dependent protein kinase IV (CaMKIV). Here, we show that CaMKIV-knockout (KO) mice developed less analgesic tolerance after chronic morphine administration with no alteration in physical dependence or acute morphine-induced analgesia. The increase in phosphorylated CREB expression observed in wild-type mice after chronic morphine was absent in CaMKIV-KO mice, while there was no difference in the expression or phosphorylation of the micro-opioid receptor between groups. Morphine-treated CaMKIV-KO mice showed less G-protein uncoupling from the micro-opioid receptor than did wild-type mice, while uncoupling was similar in control wild-type and KO mice. In addition, morphine reduced inhibitory transmission to a greater degree in CaMKIV-KO mice than in controls after chronic morphine exposure. Our results provide novel evidence for the role of CaMKIV in the development of opioid analgesic tolerance but not physical dependence.
机译：cAMP反应元件结合蛋白（CREB）是参与学习，记忆和药物成瘾的转录因子，被钙钙调蛋白依赖性蛋白激酶IV（CaMKIV）磷酸化。在这里，我们表明，在长期服用吗啡后，CaMKIV敲除（KO）小鼠的镇痛耐受性降低，而对身体依赖性或吗啡诱导的镇痛没有任何改变。 CaMKIV-KO小鼠中，慢性吗啡后在野生型小鼠中未观察到磷酸化CREB表达的增加，而各组之间的微阿片受体的表达或磷酸化没有差异。经吗啡处理的CaMKIV-KO小鼠与野生型小鼠相比，显示出与微阿片受体相比较少的G蛋白解偶联，而在对照野生型和KO小鼠中，解偶联相似。此外，在慢性吗啡暴露后，吗啡在CaMKIV-KO小鼠中的抑制传递比对照组更大程度地降低。我们的结果为CaMKIV在类阿片镇痛耐受性发展中的作用提供了新的证据，但没有物理依赖性。

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