近年来创伤后应激障碍（PTSD）发病率持续增加，但由于其发生发展的机制不清，目前防治办法有限。应激相关的恐惧记忆消退异常是PTSD发生的主要诱因之一，厘清恐惧记忆消退的生物学机制，促进其发生甚至最终将恐惧记忆从脑中完全擦除，对PTSD防治具有重要意义。我们前期对小鼠声音诱导的条件性恐惧（AFC）研究发现，在消退训练前给予一次记忆再现可将AFC记忆擦除，而基底外侧杏仁核内泛素蛋白酶体系统依赖的蛋白降解增多是主要原因。使用组织标本RNA-seq技术我们筛选到一个长链非编码RNA，uc009fca.1，发现其不仅参与恐惧记忆的擦除，并且能够改变蛋白的多泛素化修饰。基于此，本项目将结合体内、体外模型，多角度验证uc009fca.1在恐惧记忆擦除中的时空特异性作用方式和调节蛋白泛素化降解的分子机制，解析其发挥功能效应的途径及作用靶点，揭示最终哪些靶分子发生泛素化降解并通过何种方式参与恐惧记忆的擦除。

In recent years, the incidence of post-traumatic stress disorder (PTSD) has been increasing significantly. However, due to the unclear pathogenesis of PTSD, the prevention and treatment methods are limited. Many reports show that the abnormal extinction of fear memory, which caused by the traumatic stress, is one triggers for PTSD. Therefore, to clarify the biological mechanisms of fear memories extinction, promote its happening and even erase the fear memory from brain completely, are crucial for PTSD treatment. Our previous results showed that additional memory retrieval before extinction training can effectively erase the auditory cued fear conditioning (AFC), which may be related with the increase of the ubiquitin proteasome system-dependent protein degradation in the basolateral amygdala. Using RNA-seq assay, uc009fca.1, a long non-coding RNA, was screened to decrease after Retrieval+Extinction. Further studies indicated that uc009fca.1 not only involved in the erasure of fear memory but also modified the ubiquitination of proteins. Based on these findings, we will use in vivo and in vitro models to clarify the temporal and spatial effects and mechanisms of uc009fca.1 during the erasure of fear memory and protein ubiquitination from multi-angle, state the effective pathways and target molecules of uc009fca.1, reveal the final ubiquitin degraded proteins and their effect on synaptic plasticity involved in the fear memory erasure.