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.

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.

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

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.

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

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

Cation-independent-mannose-6-phosphate-receptor, or insulin-like-growth-factor-2-receptor (CIM6P/IGF2R) expressed in the hippocampus controls the protein metabolism regulated by learning and required for memory consolidation, and is also a key mechanism for memory enhancement.

Serotonin, a neurotransmitter mostly studied in relation with emotions, also plays an important role in the control of episodic memories.

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

Parvalbumin inhibitory neuron-mediated feed-forward inhibition in dentate gyrus-CA3 circuit governs time-dependent re-organization of memory traces in hippocampal-cortical networks to support systems consolidation.