Selective activation of locus coeruleus noradrenergic terminals drives anxiety-like behaviors through activation of β-adrenergic receptors in the basolateral amygdala.
Optogenetic approaches in young and aged rats define multiple roles for basolateral amygdala in guiding intertemporal choice, and show that these roles change across the lifespan.
Rat orbitofrontal cortex is required to accurately represent outcome distributions, whereas basolateral amygdala is necessary for the facilitation of learning in response to surprising events.
Sst+ interneurons drive feedforward inhibition in the basolateral amygdala, and thus provide a framework for why interneuron subtypes may mediate different archetypal circuit motifs across different brain regions.
Behavior- or optogenetic-driven activation of a basolateral amygdala projection to the nucleus accumbens enhances infralimbic cortex activity and long-term fear extinction.
Early life adversity led to hyper-innervation from the basolateral amygdala to the prefrontal cortex earlier in females than males and disrupted maturation of functional connectivity, which predicted anxiety-like outcomes.
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.
Glutamatergic projections from basolateral to central amygdala, implicated in neuropsychiatric disorders, develop rapidly during early postnatal period and their development is modulated via endogenously active kainate receptors.
Deep brain calcium imaging reveals the abnormal neuronal activity patterns of the amygdala GABAergic neurons in an animal model of human sleep disorder narcolepsy.
