On top of the temporal analysis, two brain areas known to be involved in memory formation (hippocampal CA1 region) and memory maintenance (anterior cingulate cortex, ACC) were investigated 13, 14. We chose to investigate three time-points that correspond to naïve mice (no CFC, 0 h), short-term memory formation (1 h after CFC), and memory maintenance (4 w after CFC). As a learning paradigm we chose the very robust and extremely well characterized contextual fear conditioning (CFC) paradigm 12. In an effort to obtain an unbiased, genome-wide view of chromatin modification changes during short- and long-term memory formation and maintenance we performed ChIP-, MeDIP-, and RNA-seq experiments before and after learning, with brain region and cell type-specifically, for several chromatin modifications in three month old male mice ( Fig.
![sdata tool memory duplicator sdata tool memory duplicator](https://m.media-amazon.com/images/I/61jseKkV4hL._AC_SL1500_.jpg)
In a nutshell, targeted approaches like ChIP-qPCR yield high precision but very low recall whereas genome-wide approaches like ChIP-seq usually have reduced precision but very good recall.
![sdata tool memory duplicator sdata tool memory duplicator](https://m.media-amazon.com/images/I/6117ajo1fgL._AC_SX679_.jpg)
So far, studies have primarily used ChIP-qPCR or targeted bisulfite sequencing to scrutinize promoter regions of key memory genes, an approach that is highly sensitive in detecting even small changes but lacks the profound insights into gene-regulatory networks and enhancers that whole-genome techniques could provide. These insights are further strengthened by stable and transient memory-related chromatin modification changes in learning genes such as Reelin, Calcineurin, and Bdnf 4, 7– 10. Memory-related gene activity changes most probably concur with altered chromatin states, as mutations in chromatin-modifying or chromatin-binding proteins cause learning and memory defects and many neurological and psychiatric diseases 3– 6. These changes are regulated by intracellular signaling cascades that control protein and gene activity 1, 2. A hallmark of memory-related structural changes is the strengthening or weakening of existing synapses and the formation of new ones, the so-called ‘synaptic plasticity’. The establishment and maintenance of memory is governed by structural and functional changes of memory-forming neuronal subpopulations. Learning and memory processes are crucial for an organism’s capability to adapt to environmental changes.