Abstract: The formation and preservation of long-term memories critically depend upon coordinated activity of neuronal circuits, intracellular signaling cascades and synaptic remodeling (Josselyn et al., 2015). These essential processes occur in specific cell populations known as  the engram ensemble (Josselyn et al., 2015). The current model for engram formation suggests that an experience activates a sub-population of neurons that can be measured by the expression of immediate early genes (IEG), such as Arc (activity regulated cytoskeleton associated protein, Arg3.1) or cFos (Fos Proto-Oncogene, AP-1 transcription factor subunit). Activated engram cells are then physically or chemically modified during memory consolidation, where labile memory is transformed into a more stable and long-lasting state. Notably, the memory consolidation process occurs predominantly long after the initial stimulus had ceased and the engram cells are in a dormant or a quiescent state. Reactivation of the engram ensemble by subsequent presentation of the original stimuli results in memory retrieval. Therefore, temporal progressions of memory formation from learning to retrieval require several waves of delayed transcriptional and translational alterations (Josselyn et al., 2015). Nonetheless, the molecular mechanisms that enable this temporal and spatial synchronization remain elusive.