Glucocorticoid Receptor With New Protein Synthesis To Consolidate And Subside In The Role Of The Voice Of Fear Conditioning 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' hour 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 hours 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 well known that initial consolidation requires de novo gene transcription and protein synthesis in order for memory to become stable. The consolidated memory again becomes labile and temporarily sensitive to disruption when retrieved, requiring a reconsolidation process to become permanent. Although it is well established that glucocorticoid receptor (GR) in the basolateral nucleus of amygdala (BLA) is required for consolidation of fear memory, little is known about its role in reconsolidation of fear memory. In the present study, we first examined the effect of GR blockade on post-conditioning consolidation of auditory fear memory (AFM). Intra-BLA infusion of the GR antagonist RU486 0 h post-conditioning impaired long-term AFM, leaving short-term AFM intact. RU486 had no effect if infusion was performed 6 h post-conditioning. We then investigated the effect of the RU486 treatment on post-retrieval reconsolidation of AFM. Severe amnesia took place when RU486 was infused into the BLA 0 h post-retrieval (reactivation) of AFM, regardless of whether the retrieval was performed 1 day or 10 days post-conditioning. RU486 produced no amnesia if the memory retrieval was omitted, or if the drug was administered 6 h post-retrieval. Treatment with RU486 0 h post-retrieval produced no deficit in post-retrieval short-term memory (PR-STM), but impaired post-retrieval long-term memory (PR-LTM), and the amnesia exhibited no spontaneous recovery 6 days after retrieval. The present results provide strong evidence that GR in the BLA is required for reconsolidation as well as consolidation of auditory fear memory.