Social-interaction impairment in germ-free mice is associated with a markedly altered transcriptional response to social novelty in the amygdala, as characterised by replacement of upregulation of common stimulus-induced pathways with upregulation of the splicing machinery.
Dopaminergic input shapes activity of specialized amygdala inhibitory cell clusters by ionotropic and metabotropic mechanisms that may enable their selection during distinct fear-related behavioral states.
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.
Circuit and transcriptional analysis shows that genetically defined central amygdala neurons and their projections to the ventral periaqueductal gray mediate behavioral and affective responses to pruritus.
Primate amygdala neurons provide a coordinated representation of space and motivational significance whereby amygdala responses to visual stimuli predicting either rewards or aversive stimuli could influence spatial attention in a similar manner.
When the fear-enhancing effects of prior exposure to stress are absent, the expression of fear reflects normal neural activity in the medial prefrontal cortex, not stress-induced hyperactivity in the amygdala.