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.

A new strategy of memory consolidation disruption based on astrocyte and purinergic signaling, which leads to persistent fear memory attenuation accompanied by reduced fear-related anxiety behavior.

Fear memory intensity modulates brain connectivity patterns, with stronger memories causing a pronounced reduction in interregional coordinated activity and isolation of the amygdala from other key regions.

Cholecystokinin-positive neural projection from entorhinal cortex to lateral amygdala modulates the long-term potentiation of auditory-evoked potential in lateral amygdala and underlies the formation of trace fear memory.

A fear conditioning-induced miRNA acts in a negative feedback loop that targets vesicle exocytosis and neurotransmitter receptor trafficking, and inhibits memory formation.

The anterior cingulate cortex provides predictive relationships between the context and the predator threat and influences the acquisition and expression of fear memory to predatory threat.

Cerebellar STAT3 is indispensable for proper expression of fear memory network processing.

Forgetting of remote fear memory is promoted by increased hippocampal neurogenesis only after hippocampal reactivation by long time memory retrieval.

Cerebellar-periaqueductal grey interactions contribute to fear-conditioned processes and, as such, provide a novel target for treating psychological conditions including post-traumatic stress disorder.

Activity-dependent genetic labeling during behavioral learning shows Fragile-X syndrome model mice exhibit impaired hippocampal engram reactivation, and that enriched environment experience improves fear memory retrieval by enhancing engram reactivation efficacy.