Chao Jennifer, Nestler Eric J
Department of Psychiatry and Center for Basic Neuroscience, The University of Texas, Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9070, USA.
Annu Rev Med. 2004;55:113-32. doi: 10.1146/annurev.med.55.091902.103730.
Addiction can be viewed as a form of drug-induced neural plasticity. One of the best-established molecular mechanisms of addiction is upregulation of the cAMP second messenger pathway, which occurs in many 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 DeltaFosB, 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.
成瘾可被视为药物诱导的神经可塑性的一种形式。成瘾最确定的分子机制之一是cAMP第二信使途径的上调,这种上调发生在许多神经元细胞类型中,是对长期使用阿片类药物或其他滥用药物的反应。这种上调以及由此导致的转录因子CREB的激活似乎介导了耐受性和依赖性的各个方面。相比之下,另一种转录因子DeltaFosB的诱导则产生相反的效果,可能导致对药物暴露的敏感反应。了解这些机制可能会带来更有效的成瘾性疾病治疗方法。