Social fear and avoidance of social partners and social situations represent the core behavioral symptom of Social Anxiety Disorder (SAD), a prevalent psychiatric disorder worldwide. The pathological mechanism of SAD remains elusive and there are no specific and satisfactory therapeutic options currently available. With the development of appropriate animal models, growing studies start to unravel neuronal circuit mechanisms underlying social fear, and underscore a fundamental role of the prefrontal cortex (PFC). Prefrontal cortical functions are implemented by a finely wired microcircuit composed of excitatory principal neurons (PNs) and diverse subtypes of inhibitory interneurons (INs). Disinhibition, defined as a break in inhibition via interactions between IN subtypes that enhances the output of excitatory PNs, has recently been discovered to serve as an efficient strategy in cortical information processing. Here, we review the rodent animal models of social fear, the prefrontal IN diversity, and their circuits with a particular emphasis on a novel disinhibitory microcircuit mediated by somatostatin-expressing INs in gating social fear behavior. The INs subtype distinct and microcircuit-based mechanism advances our understanding of the etiology of social fear and sheds light on developing future treatment of neuropsychiatric disorders associated with social fear.

对社交伙伴的社交恐惧和回避以及社交情境是社交焦虑症（SAD）的核心行为症状，而社交焦虑症是全球范围内的一种普遍性精神病。SAD的病理机制仍然难以捉摸，目前尚无特异性和令人满意的治疗选择。随着适当动物模型的发展，越来越多的研究开始揭示社会恐惧背后的神经元回路机制，并强调前额叶皮层（PFC）的基本作用。前额叶皮层功能是由细线微电路实现的，该电路由兴奋性主要神经元（PNs）和抑制性中间神经元（INs）的各种亚型组成。去抑制作用，定义为抑制作用的中断通过最近发现，增强兴奋性PNs输出的IN亚型之间的相互作用可作为皮质信息处理中的有效策略。在这里，我们回顾了啮齿动物的社交恐惧动物模型，前额叶IN多样性及其电路，特别着重于表达生长抑素的IN介导的社交抑制行为中介导的新型抑制性微电路。INs亚型独特且基于微电路的机制提高了我们对社会恐惧病因的理解，并为发展与社会恐惧相关的神经精神疾病的未来治疗方法提供了启示。