Risk of relapse is a major challenge in the treatment of substance use disorders. Several types of learning and memory mechanisms are involved in substance use and have implications for relapse. Associative memories form between the effects of drugs and the surrounding environmental stimuli, and exposure to these stimuli during abstinence causes stress and triggers drug craving, which can lead to relapse. Understanding the neural underpinnings of how these associations are formed and maintained will inform future advances in treatment practices. A large body of research has expanded our knowledge of how associative memories are acquired and consolidated, how they are updated through reactivation and reconsolidation, and how competing extinction memories are formed. This review will focus on the vast literature examining the mechanisms of cocaine Pavlovian associative memories with an emphasis on the molecular memory mechanisms and circuits involved in the consolidation, reconsolidation, and extinction of these memories. Additional research elucidating the specific signaling pathways, mechanisms of synaptic plasticity, and epigenetic regulation of gene expression in the circuits involved in associative learning will reveal more distinctions between consolidation, reconsolidation, and extinction learning that can be applied to the treatment of substance use disorders.

复发风险是治疗物质使用障碍的主要挑战。物质使用涉及多种类型的学习和记忆机制，并且对复发有影响。药物作用与周围环境刺激之间会形成联想记忆，禁欲期间接触这些刺激会导致压力并引发对药物的渴望，从而导致复发。了解这些关联如何形成和维持的神经基础将为治疗实践的未来进步提供信息。大量研究扩展了我们对联想记忆如何获得和巩固、它们如何通过重新激活和再巩固来更新以及如何形成竞争性灭绝记忆的知识。本综述将重点研究可卡因巴甫洛夫联想记忆机制的大量文献，重点是涉及这些记忆的巩固、再巩固和灭绝的分子记忆机制和回路。阐明特定信号通路、突触可塑性机制和关联学习所涉及回路中基因表达的表观遗传调控的其他研究将揭示巩固、再巩固和消退学习之间的更多区别，可用于治疗物质使用障碍。