Protein kinases and addiction.
Protein kinases and addiction.
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DOI：
10.1196/annals.1441.022
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发表时间：
2008-10
影响因子：
5.2
通讯作者：
Messing RO
中科院分区：
文献类型：
--
作者：
Lee AM;Messing RO
尽管滥用药物有不同的化学结构，并与不同的蛋白质靶点相互作用，但它们似乎都篡夺了调节奖赏和动机的共同神经系统。成瘾是一种复杂的疾病，被认为与药物引起的突触可塑性改变有关，这是由于细胞信号、基因转录和蛋白质合成的改变。最近的证据表明，滥用药物与包括特定蛋白激酶子集的常见信号通路网络相互作用并改变。本文综述了细胞外信号调节蛋白激酶、cAMP依赖蛋白激酶、细胞周期蛋白依赖性蛋白激酶5、蛋白激酶C、钙/钙调蛋白依赖性蛋白激酶II和Fyn酪氨酸激酶的研究进展。这些激酶与药物成瘾的各个方面有关，包括急性药物效应、药物自我给药、戒断、强化、敏化和耐受。确定导致成瘾状态的蛋白激酶底物和信号通路可能为治疗药物成瘾的新的药物辅助疗法提供新的途径。
Although drugs of abuse have different chemical structures and interact with different protein targets, all appear to usurp common neuronal systems that regulate reward and motivation. Addiction is a complex disease that is thought to involve drug-induced changes in synaptic plasticity due to alterations in cell signaling, gene transcription, and protein synthesis. Recent evidence suggests that drugs of abuse interact with and change a common network of signaling pathways that include a subset of specific protein kinases. The best studied of these kinases are reviewed here and include extracellular signal-regulated kinase, cAMP-dependent protein kinase, cyclin-dependent protein kinase 5, protein kinase C, calcium/calmodulin-dependent protein kinase II, and Fyn tyrosine kinase. These kinases have been implicated in various aspects of drug addiction including acute drug effects, drug self-administration, withdrawal, reinforcement, sensitization, and tolerance. Identifying protein kinase substrates and signaling pathways that contribute to the addicted state may provide novel approaches for new pharma-cotherapies to treat drug addiction.
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