Synaptic correlates of fear extinction in the amygdala

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Abstract
The mechanisms underlying fear extinction remain unclear. Here, the authors show that extinction enhances basolateral amygdala inputs about conditioned stimuli to intercalated cells, resulting in the inhibition of fear output central amygdala neurons. These changes required medial prefrontal activity during extinction training, but, once induced, could be expressed without prefrontal inputs. Anxiety disorders such as post-traumatic stress are characterized by an impaired ability to learn that cues previously associated with danger no longer represent a threat. However, the mechanisms underlying fear extinction remain unclear. We found that fear extinction in rats was associated with increased levels of synaptic inhibition in fear output neurons of the central amygdala (CEA). This increased inhibition resulted from a potentiation of fear input synapses to GABAergic intercalated amygdala neurons that project to the CEA. Enhancement of inputs to intercalated cells required prefrontal activity during extinction training and involved an increased transmitter release probability coupled to an altered expression profile of ionotropic glutamate receptors. Overall, our results suggest that intercalated cells constitute a promising target for pharmacological treatment of anxiety disorders.