GluA1 phosphorylation at serine 831 in the lateral amygdala is required for fear renewal

摘要: Fear renewal, a widely pursued model of post-traumatic stress disorder and phobias, refers to the context-specific relapse conditioned fear after extinction. However, its molecular mechanisms are largely unknown. We found that renewal-inducing stimuli, generally believed be insufficient induce synaptic plasticity, enhanced excitatory strength, activity GluA2-lacking AMPA receptors Ser831 phosphorylation surface GluA1 in lateral nucleus amygdala (LAn) fear-extinguished rats. Consistently, induction threshold for LAn potentiation was considerably lowered extinction, renewal occluded this low-threshold potentiation. The (a potential cellular substrate renewal), but not long-term potentiation, attenuated by dialysis into neurons GluA1-derived peptide competes with Ser831-phosphorylated GluA1. Microinjections same learning. Our findings suggest constitutes promising target clinical treatment aberrant fear-related disorders.