基底外侧杏仁核（BLA）是调控海洛因成瘾与线索记忆的关键核团，然而其神经元内组蛋白乙酰化修饰对成瘾记忆的调控作用却鲜有报道。本课题利用小鼠海洛因位置偏爱和条件奖赏模型分别模拟成瘾环境及事件线索，透射电镜获得BLA神经元突触可塑性证据；RT-PCR、Western blot、免疫荧光等技术筛选在海洛因成瘾记忆中发挥关键作用的组蛋白乙酰化修饰酶；进而利用过表达或shRNA干预关键酶活性，观察成瘾不同阶段行为改变，明确关键酶对海洛因成瘾记忆的调控作用；利用染色质免疫沉淀等技术检测关键酶调控的记忆相关靶基因，揭示关键酶的下游调控通路；利用ACPC、MK-801干预NMDA受体功能，检测NR1-CaMKII-CREB通路激活及关键酶表达，揭示关键组蛋白乙酰化修饰酶的上游调控机制。本课题不仅有助于阐明BLA中组蛋白乙酰化调控海洛因成瘾记忆的分子机制，也将为海洛因成瘾治疗新靶点提供实验证据与理论依据。

The basolateral amygdala (BLA) is a crucial nucleus that regulating the heroin addiction and cue-associated memories. However, the regulatory effect of histone acetylation on heroin addiction memory has not yet been elucidated. The present study using a mouse model of heroin-induced condition place preference and conditioned rewarding to simulate the environmental and event cues, respectively. Obtain the correlative changes of synaptic plasticity in BLA neurons by using the transmission electron microscope. Screening the key histone acetylation/deacetylation enzymes, which play crucial roles in heroin addiction memory, by using RT-PCR, Western blot and immunofluorescence techniques. Then, use the gene over expression or shRNA methods to manipulate the activities of key enzymes during different stages of heroin addiction, and observe the correlative behavior changes, identify the regulatory effects of the key enzyme on addiction memory. Reveal the downstream pathway of the key enzyme by using the chromatin immunoprecipitation to detect the expression of memory related target genes. Use ACPC and MK-801 to activate or inhibit the NMDA receptor function, then detect the activation of NR1-CaMKII-CREB pathway and the key enzyme expression, which shall reveal the upstream regulatory mechanism of the key enzyme. The present study could not only clarify the molecular mechanisms of histone acetylation in BLA underlying heroin addiction memory, but also provide valuable experimental evidence and theoretical basis for the development of new treatment target in heroin addiction.