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Knowledge plays a central role in human life. Indeed, we are who we are largely because of what we learn and what we remember. Our knowledge structure (‘schema’) consists of our past experiences and facts stored in our long-term memory. We use our schemas to organize current knowledge and provide a framework for future understanding. A key but poorly understood issue is how the memories of everyday events initially stored in the hippocampus are ‘selected’ and then ‘assimilated’ into a relevant schema in the neocortex.

Selective retention can be triggered by novelty-induced dopamine release in the hippocampus. We made a ground-breaking finding (Takeuchi et al.Nature, 2016): projections from the noradrenergic locus coeruleus to the hippocampus can drive the novelty-induced memory enhancement via a non-canonical release of dopamine. This study also raises a possibility that the impact of distinct novel experiences that bear only minimal relationship to past experiences (‘distinct novelty’) may differ from novel experiences that share some commonality with past ones (‘common novelty’) (Yamasaki and Takeuchi, Neural Plasticity, 2017; Duszkiewicz et al.Trends Neurosci, In press). We now propose that memory of events accompanied by novelty can be selectively retained through two distinct dopaminergic mechanisms, depending on the nature of the novel experience itself.

Selected new memories can assimilate into the neocortical schema very rapidly if the relevant schema is already learned (Tse et al.Science, 2007). The functional mapping with immediately-early gene expression indicated that medial neocortical structures (the prelimbic, the anterior cingulate and anterior region of the retrosplenial cortices)-hippocampal connectivity was strongly associated with successful assimilation of new information into the relevant schema (Tse, Takeuchi et al., Science, 2011; Takeuchi and Tamura, unpublished). Pharmacological interventions established that there was parallel memory encoding in the neocortex, including the prelimbic cortex, through NMDA (N-methyl-D-aspartate)-type glutamate receptor-dependent plasticity mechanisms during the hippocampal-dependent learning of new information against the backdrop of a schema (Tse, Takeuchi et al., Science, 2011).

Understanding the neural mechanisms of selective retention and assimilation of selected new memories into relevant schema may bring us towards a more effective and consciously aimed behavioural schema therapy as well as provide suggestions for better teaching and learning strategies.