Social buffering occurs when the presence of a companion attenuates the physiological and/or behavioral effects of a stressful or fear-provoking event. It represents a way in which social interactions can immediately and potently modulate behavior. As such, social buffering is one mechanism by which strong social support increases resilience to mental illness. Although the behavioral and neuroendocrine impacts of social buffering are well studied in multiple species, including humans, the neuronal underpinnings of this behavioral phenomenon remain largely unexplored. Previous work has shown that the infralimbic prefrontal cortex (IL-PFC) is important for processing social information and, in separate studies, for modulating fear and anxiety. Thus, we hypothesized that socially active cells within the IL-PFC may integrate social information to modulate fear responsivity. To test this hypothesis, we employed social buffering paradigms in male and female mice. Similar to prior studies in rats, we found that the presence of a cagemate reduced freezing in fear- and anxiety-provoking contexts. In accordance with previous work, we demonstrated that interaction with a novel or familiar conspecific induces activity in the IL-PFC as evidenced by increased immediate early gene (IEG) expression. We then utilized an activity-dependent tagging murine line, the ArcCreERT2 mice, to express channelrhodopsin (ChR2) in neurons active during the social encoding of a new cagemate. We found that optogenetic reactivation of these socially active neuronal ensembles phenocopied the effects of cagemate presence in male and female mice in learned and innate fear contexts without being inherently rewarding or altering locomotion. These data suggest that a social neural ensemble within the IL-PFC may contribute to social buffering of fear. These neurons may represent a novel therapeutic target for fear and anxiety disorders.

中文翻译：

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前额社会神经集合的光遗传学激活模仿了恐惧的社会缓冲。

当同伴的存在减弱了压力或挑衅事件的生理和/或行为影响时，就会发生社会缓冲。它代表了一种社交互动可以立即有效地调节行为的方式。这样，社会缓冲是一种机制，通过这种机制，强大的社会支持可以增强对精神疾病的适应力。尽管社会缓冲对行为和神经内分泌的影响在包括人类在内的多个物种中都得到了很好的研究，但这种行为现象的神经基础仍未得到充分研究。先前的研究表明，下肢前额叶皮层（IL-PFC）对于处理社会信息以及在单独的研究中对于调节恐惧和焦虑非常重要。从而，我们假设IL-PFC中的社交活跃细胞可能整合社交信息以调节恐惧反应性。为了验证这一假设，我们在雄性和雌性小鼠中采用了社会缓冲范式。与大鼠先前的研究相似，我们发现，在恐惧和焦虑引起的情况下，鼠笼的存在降低了冻结。根据以前的工作，我们证明了与新颖或熟悉的同种异体的相互作用诱导了IL-PFC中的活性，这由立即早期基因（IEG）表达增加所证明。然后，我们利用了一种依赖于活动的标记鼠系ArcCreERT2小鼠，在新笼伴侣的社会编码过程中，在活跃的神经元中表达了视紫红质素（ChR2）。我们发现，这些社交活动神经元集合的光遗传学激活表型复制了习性和先天恐惧情况下雄性和雌性小鼠中笼状动物存在的影响，而没有内在地奖励或改变运动。这些数据表明，IL-PFC中的社交神经集合可能有助于恐惧的社交缓冲。这些神经元可能代表恐惧和焦虑症的新型治疗靶标。