A new memory is stabilized through a process of consolidation, which is known to depend on a critical phase of protein synthesis. Consolidated memories are widely believed to be stable and resilient to disruption. This belief, however, has been recently challenged by studies showing that established memories become labile when reactivated and, furthermore, require another phase of protein synthesis to be maintained. Although this process has been termed """"""""re-consolidation"""""""", it is not known whether it is, in fact, a true recapitulation of consolidation. Very little is known about the underlying mechanisms and the specific functions of memory reconsolidation. This knowledge is not only essential for the understanding of how memory works, but it will also contribute to the development of novel strategies for treating psychiatric conditions based on traumatic memories (i.e. post-traumatic stress disorders, phobias and depression) and novel approaches for increasing memory strength. In this project, we propose to use a fear-conditioned-based task (inhibitory avoidance, IA) and molecular investigations to carry out a comparative multiple level analysis of the anatomical and temporal molecular requirements of memory consolidation and reconsolidation.
Our Aims are to determine to what extent both consolidation and reconsolidation involve the same molecules and brain areas (circuits) with similar temporal dynamics and to test the functional roles and the contribution of modulation on memory reconsolidation. The results of this project should provide important information for developing new strategies for the pharmacotherapeutic intervention of cognitive disorders caused by traumatic memories (i.e. PTSD, phobias, addiction and depression) and debilitating conditions of memory loss such as those occurring in aging and Alzheimer's Disease.
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