Kalivas Peter W
Department of Neurosciences, Medical University of South Carolina. Charleston, South Carolina 29425, USA.
Am J Addict. 2007 Mar-Apr;16(2):71-8. doi: 10.1080/10550490601184142.
The development of pharmacotherapies for cocaine addiction has been disappointingly slow. However, new neurobiological knowledge of how the brain is changed by chronic pharmacological insult with cocaine is revealing novel targets for drug development. Certain drugs currently being tested in clinical trials tap into the underlying cocaine-induced neuroplasticity, including drugs promoting GABA or inhibiting glutamate transmission. Armed with rationales derived from a neurobiological perspective that cocaine addiction is a pharmacologically induced disease of neuroplasticity in brain circuits mediating normal reward learning, one can expect novel pharmacotherapies to emerge that directly target the biological pathology of addiction.
用于治疗可卡因成瘾的药物疗法进展一直令人失望地缓慢。然而，关于大脑如何因长期使用可卡因受到药理损伤而发生变化的新神经生物学知识，正在揭示药物开发的新靶点。目前正在临床试验中测试的某些药物利用了可卡因诱导的潜在神经可塑性，包括促进γ-氨基丁酸（GABA）或抑制谷氨酸传递的药物。基于从神经生物学角度得出的理论依据，即可卡因成瘾是一种在介导正常奖赏学习的脑回路中由药理学诱导的神经可塑性疾病，人们可以期待出现直接针对成瘾生物学病理的新型药物疗法。
