Abstract
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as post-traumatic stress are characterized by an impaired ability to learn that cues previously associated with danger no longer represent a threat.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. Here we show in rats that extinction is associated with increased levels of synaptic inhibition in fear output neurons of the central amygdala (CEA). This increased inhibition results from a potentiation of fear input synapses to GABAergic intercalated amygdala neurons that project to CEA. Enhancement of inputs to intercalated cells required prefrontal activity during extinction training and involved a higher 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 treatments aiming to facilitate the treatment of anxiety disorders.
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