A novel behavioral paradigm is described that permanently attenuates fear memories in rats by destabilizing and reinterpreting them as safe through an isolated retrieval trial before extinction training. This approach avoids the need for drugs and prevents the return of fear through mechanisms such as renewal, reinstatement, and spontaneous recovery. The study shows that when an isolated retrieval trial is conducted within the reconsolidation window, extinction training leads to a lasting revaluation of the conditioned stimulus (CS) as less threatening, reducing fear responses. In contrast, extinction training outside the reconsolidation window does not produce such long-term effects. The study also examines the molecular mechanisms underlying this effect, finding that the phosphorylation of GluR1 receptors at ser845 is involved in the destabilization of fear memories during reconsolidation. This process is followed by dephosphorylation of GluR1, which may underlie the long-term reduction in fear responses. The results suggest that the reconsolidation process allows for the updating of fear memories, leading to a more enduring reduction in fear compared to traditional extinction training. The findings indicate that the reconsolidation window is critical for the effectiveness of the paradigm, as the interval between retrieval and extinction training significantly affects the outcome. The study also highlights the potential clinical implications of this approach, suggesting that it could be used to treat anxiety-related disorders by preventing the re-emergence of fear memories. Future research aims to determine whether this procedure can render a once-fear-inducing stimulus neutral or safe, and to further clarify the distinction between fear expression and fear memory in response to this treatment.A novel behavioral paradigm is described that permanently attenuates fear memories in rats by destabilizing and reinterpreting them as safe through an isolated retrieval trial before extinction training. This approach avoids the need for drugs and prevents the return of fear through mechanisms such as renewal, reinstatement, and spontaneous recovery. The study shows that when an isolated retrieval trial is conducted within the reconsolidation window, extinction training leads to a lasting revaluation of the conditioned stimulus (CS) as less threatening, reducing fear responses. In contrast, extinction training outside the reconsolidation window does not produce such long-term effects. The study also examines the molecular mechanisms underlying this effect, finding that the phosphorylation of GluR1 receptors at ser845 is involved in the destabilization of fear memories during reconsolidation. This process is followed by dephosphorylation of GluR1, which may underlie the long-term reduction in fear responses. The results suggest that the reconsolidation process allows for the updating of fear memories, leading to a more enduring reduction in fear compared to traditional extinction training. The findings indicate that the reconsolidation window is critical for the effectiveness of the paradigm, as the interval between retrieval and extinction training significantly affects the outcome. The study also highlights the potential clinical implications of this approach, suggesting that it could be used to treat anxiety-related disorders by preventing the re-emergence of fear memories. Future research aims to determine whether this procedure can render a once-fear-inducing stimulus neutral or safe, and to further clarify the distinction between fear expression and fear memory in response to this treatment.