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

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

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

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.

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.

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

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

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.

Dorsal paired medial neurons, which are required for memory consolidation, promote sleep by inhibiting the excitation of mushroom body neurons.