Reactivation of consolidated memories can induce a labile period, in which these reactivated memories might be susceptible to change and need reconsolidation. Prediction error (PE) has been recognized as a necessary boundary condition for memory destabilization. Moreover, memory strength is also widely accepted as an essential boundary condition to destabilize fear memory. This study investigated whether different strengths of conditioned fear memories require different degrees of PE during memory reactivation in order for the memories to become destabilized. Here, we assessed the fear-potentiated startle and skin conductance response, using the post-retrieval extinction procedure. A violation of expectancy (PE) was induced during retrieval to reactivate enhanced (unpredictable-shock) or ordinary (predictable-shock) fear memories that were established the day before. Results showed that a PE retrieval before extinction can prevent the return of predictable-shock fear memory but cannot prevent the return of unpredictable-shock fear memory, indicating that a single PE is insufficient to destabilize enhanced fear memory. Therefore, we further investigated whether increasing the degree of PE could destabilize enhanced fear memory using different retrieval strategies (multiple PE retrieval and unreinforced CS retrieval). We found that spontaneous recovery of enhanced fear memory was prevented in both retrieval strategies, but reinstatement was only prevented in the multiple PE retrieval group, suggesting that a larger amount of PE is needed to destabilize enhanced fear memory. The findings suggest that behavioral updating during destabilization requires PE, and the degree of PE needed to induce memory destabilization during memory retrieval depends on the strength of fear memory. The study indicates that memory reconsolidation inference can be used to destabilize stronger memories, and the findings shed lights on the treatment of posttraumatic stress disorders and anxiety disorders.

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Counter-empathy significantly affects people’s social lives. Previous evidence indicates that the degree of counter-empathy can be either strong or weak. Strong counter-empathy easily occurs when empathizers are prejudiced against the targets of empathy (e.g. prejudice against outgroup members) and activates brain regions that are opposite to those activated by empathy. Weak counter-empathy may have different neural processing paths from strong ones, but its underlying neural mechanisms remain unclear. In this work, we used an unfair distribution paradigm, which can reduce participants’ prejudice against persons empathized with, and functional magnetic resonance imaging to explore the neural mechanisms underlying counter-empathy. Here, empathy and counter-empathy shared a common neural mechanism, induced by unfair distribution, in the right middle temporal gyrus. Counter-empathy activated distinct brain regions that differed from those of empathic responses in different situations. The functions of these brain regions, which included the middle frontal, middle temporal and left medial superior gyri, were similar and mostly related to emotional regulation and cognitive processing. Here, we propose a process model of counter-empathy, involving two processing paths according to whether or not prejudice exists. This study has theoretical significance and broadens our understanding of the cognitive neural mechanisms underlying empathy and counter-empathy.

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