Protein synthesis inhibition in the basolateral nucleus of amygdala facilitates extinction of auditory fear memory  

作　　者：JIN XinChun QI XueLian YANG XiaoFei LI BaoMing 

机构地区：[1]Institute of Neurobiology, Institutes of Brain Science, Fudan University, Shanghai 200032, China [2]State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Fudan University, Shanghai 200032, China [3]Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

出　　处：《Chinese Science Bulletin》2007年第18期2532-2542,共11页

基　　金：Supported by grants to Bao-Ming Li from the Ministry of Science and Technology of China (Grant No. 2006CB500807);the Ministry of Education of China (Program for Changjiang Scholars and Innovative Research Team in University);the National Natural Science Foundation of China (Grant Nos. 30225023, 30430240 and 30611120530)

摘　　要：It is known that consolidation of fear conditioning requires de novo protein synthesis in the amygdala. However, there is controversy about the role of protein synthesis in post-retrieval extinction of fear memory. The present study investigated the effect of protein synthesis inhibition (PSI) in the baso- lateral nucleus of amygdala (BLA) on post-retrieval extinction of auditory fear memory. Intra-BLA infu- sion of the protein synthesis inhibitor anisomycin ‘0’ h post-retrieval facilitated the extinction, but was ineffective if the memory was not retrieved. Anisomycin had no effect on the extinction when it was infused 6 h post-retrieval. The present results suggest that there exists a protein-synthesis-dependent mechanism in the BLA that retards extinction of auditory fear memory.It is known that consolidation of fear conditioning requires de novo protein synthesis in the amygdala. However, there is controversy about the role of protein synthesis in post-retrieval extinction of fear memory. The present study investigated the effect of protein synthesis inhibition （PSI） in the basolateral nucleus of amygdala （BLA） on post-retrieval extinction of auditory fear memory. Intra-BLA infusion of the protein synthesis inhibitor anisomycin ‘0＇ h post-retrieval facilitated the extinction, but was ineffective if the memory was not retrieved. Anisomycin had no effect on the extinction when it was infused 6 h post-retrieval. The present results suggest that there exists a protein-synthesis-dependent mechanism in the BLA that retards extinction of auditory fear memory.

关 键 词：蛋白质合成 扁桃体 听觉 衰退 

分 类 号：R338.3[医药卫生—人体生理学]