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.

Single-unit activity in the ventrolateral periaqueductal gray, a brain region implicated in organizing fear output, is found to reflect threat probability, a more versatile threat signal.

Comprehensive behavioral ethograms reveal a fear conditioned cue to elicit a temporally organized suite of behaviors spanning freezing, locomotion, rearing, and jumping.

Direct reprogramming of somatic cells to an inner ear sensory hair cell-like state provides an experimental platform to identify causes and treatments for hair cell loss and hearing deficits.

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.

Inhibition of activity in the right frontal eye fields reduces the amplifying effect of gaze in value-based choice.

Enteric bacteria associated with bloodstream infections are attracted to human serum through L-serine and the chemoreceptor Tsr, and in an enterohemorrhagic lesion model use chemotaxis to invade damaged vasculature.

Direct- and indirect pathway neurons of the posterior striatum display divergent in vivo and ex vivo plasticity after fear learning, and differentially modulate defensive behaviors displayed in the presence, and absence of threat-predicting sensory cues.

Early life adversity (ELA) accelerated PV+ interneuron development in BLA and delayed the ability of pre-adolescent mice to express, but not form, an auditory conditioned fear memory in childhood.