State anxiety is common in our life and has a significant impact on our emotion, cognition and behavior. Previous studies demonstrate that people in a negative mood are associated with low sympathy and high personal distress. However, it is unknown how state anxiety regulates empathic responses so far. Here, we recorded event-related brain potentials (ERP) from the experimental group who were in state anxiety and the control group when they were watching painful and neutral pictures. Participants in the experimental group and the control group were asked to do the same mental arithmetic problems. The only difference was that the experimental group had time restriction and was evaluated by the observer. The results showed that no significant N2 differentiation between painful and neutral stimuli was found in both groups. In contrast, LPP amplitudes induced by painful stimuli were significantly larger than that of neutral stimuli in the control group, but not in the experimental group. Our results indicate that state anxiety inhibit empathic responses from the early emotional sharing stage to the late cognitive evaluation stage. It provides neuroscientific evidence that one’s own emotional state will have an important impact on empathy.

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Previous studies have found that individuals exhibit empathic responses when others are treated unfairly. However, there remains a lack of clarity over the extent to which self-interest regulates these empathic responses, and in identifying which component of empathy is more likely to be affected. To investigate these issues, an experiment was designed based on a money distribution task with two conditions [observation condition (OC) vs. participation condition (PC)], and carried out using scalp-recorded event-related potentials (ERPs). Behavioral data showed that the participants’ empathic responses were consistent with their coplayers’ emotional expressions in the OC, whereas they were inconsistent with the coplayers’ expressions in the PC. The electrophysiological data showed that the neural encoding of facial expressions (reflected in the N170) was not affected by self-interest. However, the late stage of empathic responses (LPP) showed a decline when participants’ self-interest was involved. Disadvantageous inequality and relatively fair distribution to others elicited a more pronounced feedback-related negativity (FRN) than advantageous inequality distribution in both the OC and PC. As the late stage of empathic responses is also indexed by the LPP amplitude, these results indicate that the participants were more concerned for their own outcomes than for others’ benefits when self-interest was involved, which reduced their empathy toward their coplayers at the late stage of empathic responses.

Previous studies have widely reported that competition modulates an individual’s ability to empathize with pain experienced by others. What remains to be clarified, however, is how modulations in the intensity of competition might affect this type of empathy. To investigate this, we first used a Eriksen Flanker task to set different competitive intensity context (high competitive intensity, HCI; medium competitive intensity, MCI; low competitive intensity, LCI). Then we used a recognition task as a competitive task, in which we recorded event-related potentials (ERP) while participants viewed static images of body parts in painful and non-painful situations. Participants were informed that both sets of images depicted an opponent that they were required to play against in the recognition task that varied in levels of competitive intensity according to condition (HCI, MCI, and LCI). We observed an early N2 differentiation between pain and no-pain stimuli over the frontal area under MCI and LCI conditions, but this was not detected under HCI condition. Moreover, we observed a pattern of pain and no-pain differentiation for the late LPP over the frontal and centro-parietal regions under HCI, MCI, and LCI condition. As the pain empathy response is indexed by pain and no-pain differentiation, these results indicate a down-regulation of pain empathy response attributable to a high level of competition. With its very early onset, this effect appears to inhibit bottom-up processing of the ability to perceive pain experienced by an opponent. Our results provide neuroscientific evidence for a deficit in early automatic arousal in response to the pain of the opponent under the influence of high competitive intensity.

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.