Molecular neurobiology of addiction
Molecular neurobiology of addiction
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DOI：
10.1080/105504901750532094
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发表时间：
2001-06-01
影响因子：
3.7
通讯作者：
Nestler, EJ
中科院分区：
文献类型：
--
作者：
Nestler, EJ
成瘾可以被看作是药物诱导的神经可塑性的一种形式。成瘾的最佳建立的分子机制之一是cAMP第二信使途径的上调，其发生在人类神经元细胞类型中，以响应阿片类药物或其他滥用药物的长期施用。转录因子CREB的这种上调和由此产生的激活似乎介导了耐受性和依赖性。相反，诱导另一种转录因子，称为Delta FosB，发挥相反的作用，并可能有助于对药物暴露的敏感反应。了解这些机制可能会导致更有效的治疗成瘾性疾病。
Addiction can be viewed as a form of drug-induced neural plasticity. One of The best established molecular mechanisms of addiction is the upregulation of the cAMP second messenger pathway, which occurs in man, neuronal cell types in response to chronic administration of opiates or other drugs of abuse. This upregulation and The resulting activation of the transcription factor CREB appear to mediate aspects of tolerance and dependence. In contrast, induction of another transcription factor, termed Delta FosB, exerts the opposite effect and may contribute to sensitized responses to drug exposure. Knowledge of these mechanisms could lead to more effective treatments for addictive disorders.