Abstract

<p id="C2">Extinction training that occurs shortly after fear conditioning fails to yield long-term extinction memory, a phenomenon that is known as the immediate extinction deficit (IED). The IED may be linked to levels of stress at the onset of extinction training and event segmentation. Under high levels of stress, the consolidation of extinction memory is impaired, resulting in the IED. Under moderate or low levels of stress, immediate extinction would be effective but susceptible to event segmentation. The neurobiological mechanisms of IED may involve stress-induced activation of the locus coeruleus norepinephrine system, which leads to hyperexcitability of the basolateral amygdala and the subsequent inhibition of activity of the medial prefrontal cortex (i.e., a region that plays a central role in fear extinction) through synaptic projections. Future studies should consider long-term outcomes of the IED and optimization of the clinical application of immediate extinction.

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