The ability to infer others’ mental states is essential to social interactions. This ability, critically evaluated by testing whether one attributes false beliefs (FBs) to others, has been considered to be uniquely hominid and to accompany the activation of a distributed brain network. We challenge the taxon specificity of this ability and identify the causal brain locus by introducing an anticipatory-looking FB paradigm combined with chemogenetic neuronal manipulation in macaque monkeys. We find spontaneous gaze bias of macaques implicitly anticipating others’ FB-driven actions. Silencing of the medial prefrontal neuronal activity with inhibitory designer receptor exclusively activated by designer drugs (DREADDs) specifically eliminates the implicit gaze bias while leaving the animals’ visually guided and memory-guided tracking abilities intact. Thus, neuronal activity in the medial prefrontal cortex could have a causal role in FB-attribution-like behaviors in the primate lineage, emphasizing the importance of probing the neuronal mechanisms underlying theory of mind with relevant macaque animal models.

推断他人心理状态的能力对于社交互动至关重要。通过测试一种能力是否将错误信念（FB）归因于另一种能力，对该能力进行了严格评估，该能力被认为具有独特的人格魅力，并伴随着分布式大脑网络的激活。我们通过引入具有前瞻性的FB范例并结合猕猴中的化学遗传神经元操作，来挑战这种能力的分类单元特异性，并确定病因脑源。我们发现猕猴的自发凝视偏见隐含地预见了其他人的FB驱动行为。使用专门设计的药物（DREADDs）独家激活的抑制性专门设计的受体来沉默内侧前额神经元的活动，可以特别消除内在的凝视偏见，同时保持动物的视觉指导和记忆指导的追踪能力。