The overactivation of noradrenergic inputs to the amygdala during severe fear learning increases memory stability at the expense of lability, rendering the trace resistant to memory destabilization and reconsolidation.

The consolidation of newly acquired motor skills induces a functional reorganization of sequential information representations within secondary motor cortex, basal ganglia and hippocampus.

Behavioral and synaptic investigations of long-term memory in Aplysia reveal differing roles for DNA methylation, protein synthesis during training and protein synthesis shortly after training with respect to memory consolidation and maintenance.

The brain inhibits the formation of new memories just after waking to safeguard the ongoing stabilization of existing memories during sleep.

Odor cues in sleep evoke content-specific signatures of neural reactivation in visual and prefrontal brain areas that predict subsequent memory performance in the wake state.

Inhibition of 5-HT neurons in the dorsal raphe nuclei or 5-HT terminals in the anterior cingulate cortex decreased consolation-like behaviors and reduced sociability.

Retrieval enhances fear memory through reconsolidation by activating calcineurin-induced protein degradation and CREB-mediated gene expression in amygdala, hippocampus, and mPFC.

Human learners’ memory for generalities across individual items biased memory for these items after 1 month.

Prelimbic cortical inputs are differentially recruited during early memory consolidation, with claustrum projections involved at encoding and insular cortex projections recruited for recent recall.

Electrophysiological and behavioural experiments reveal that parvalbumin interneuron-mediated increases in neocortical-hippocampal interactions are necessary for successful memory consolidation.