Enhancement of fear memory by retrieval through reconsolidation.
Enhancement of fear memory by retrieval through reconsolidation.
复制标题
通过重新整合通过检索来增强恐惧记忆。
作者:
Fukushima H;Zhang Y;Archbold G;Ishikawa R;Nader K;Kida S
Memory retrieval is considered to have roles in memory enhancement. Recently, memory reconsolidation was suggested to reinforce or integrate new information into reactivated memory. Here, we show that reactivated inhibitory avoidance (IA) memory is enhanced through reconsolidation under conditions in which memory extinction is not induced. This memory enhancement is mediated by neurons in the amygdala, hippocampus, and medial prefrontal cortex (mPFC) through the simultaneous activation of calcineurin-induced proteasome-dependent protein degradation and cAMP responsive element binding protein-mediated gene expression. Interestingly, the amygdala is required for memory reconsolidation and enhancement, whereas the hippocampus and mPFC are required for only memory enhancement. Furthermore, memory enhancement triggered by retrieval utilizes distinct mechanisms to strengthen IA memory by additional learning that depends only on the amygdala. Our findings indicate that reconsolidation functions to strengthen the original memory and show the dynamic nature of reactivated memory through protein degradation and gene expression in multiple brain regions. DOI: http://dx.doi.org/10.7554/eLife.02736.001 Video cameras allow us to record events as they happen. When we look back at a video clip, what we see is an exact replica of what was originally recorded. We tend to assume that our memories work in a similar manner. However, recent research suggests that our memories may be more malleable than we realize. Once a memory has been reactivated, it goes through a process known as reconsolidation that can make it stronger or weaker, or that can change its content. Now, Fukushima et al. have carried out a series of experiments which shed light on the process of memory reconsolidation. Mice were trained to remember a negative event, and later tested on their memory of this event. Some of the mice were also given a ‘reactivation’ session, during which they were reminded of the original memory. These mice were more fearful of the event during the memory test than those who had not been reminded of it. This suggests that the process of reconsolidating the memory after it had been retrieved had the effect of making the memory stronger. Fukushima et al. then demonstrated that this enhancement depended on the synthesis of proteins in particular regions of the brain. When the mice were given an injection to block protein synthesis immediately after reactivation of the memory, their memory of the negative event was weakened. Crucially, this effect only happened when the injection was given immediately after reactivation of the memory; if the memory had not been reactivated, the injection did not change its strength. Fukushima et al. went on to show that three regions of the brain—the amygdala, the hippocampus, and the medial prefrontal cortex—are involved in memory enhancement. However, only one of them, the amygdala, is involved in the other aspects of reconsolidation. This research could support clinical work by elucidating the potential role of reconsolidation in conditions such as post-traumatic stress disorder. DOI: http://dx.doi.org/10.7554/eLife.02736.002