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Recent studies implied that AMPA receptor(AMPAR)may contribute to the changes in synaptic plasticity of lateral amygdala(LA)and nuclear accumbens in the brain.However,the exact relationship between the surface expression of AMPAR and fear memory or cocaine withdrawn remains unknown.In this study,we demonstrated that the upregulation of N-ethylmaleimide-sensitive factor(NSF)-GluR2 interactions after withdrawal from cocaine was associated with the changes in the expression of behavioral sensitization.Disruption of NSF-GluR2 interactions in the NAc increased the locomotor response of rats to cocaine by decreasing GluR2 surface insertion.In contrast,prevention of GluR2-containing AMPARs removal from synapses attenuated the expression of behavioral sensitization.Similarly,treatment with the nitric oxide donor SNAP attenuated the expression of locomotor sensitization by promoting GluR2 surface expression.In addition,we found that exogenous norepinephrine impaired LTD by increasing the phosphorylation and surface delivery of GluR1 in LA.Intraperitoneal(i.p.)injection of propranolol attenuated the reactivation-induced strengthening of fear memory retention,surface expression of GluR1 and impairment of long-term depression(LTD)in LA.Overexpression of GluR1-C-tail in amygadala attenuated reactivation-induced surface expression of GluR1,impairment of LTD and enhanced fear memory retention in rats.These findings uncover the mechanism for the role of surface stability of AMPA receptor in the fear memory retention and cocaine withdrawn.