Structural, Synaptic, and Epigenetic Dynamics of Enduring Memories

Figure 1

Schematic illustrating three essential mechanisms that might contribute to remote memory storage and thus memory endurance in the (rodent) brain, which are discussed in this review. First, during memory allocation, learning induces the activity of a specific subpopulation of cells—likely spread across different brain areas—which will become recruited into the memory trace. The amygdala (AMY), the hippocampus (HPC), and the prefrontal cortex (PFC) are known to be activated during memory allocation (for details see text). Second, in cells allocated to a specific memory—also known as the memory engram [1–3]—structural changes at the level of dendritic spines have been demonstrated by several studies. These changes are exclusive to the cells of the memory trace or engram (red) but not observed in other cells (grey) [53]. Third, memory engram cells are also likely to be characterized by epigenetic changes, such as posttranslational modifications (PTMs) on histone proteins, and methylation of the DNA, the core chromatin constituents. Note, however, that such engram-specific engagement of epigenetic mechanisms remains to be experimentally demonstrated.