Abstract

The retrosplenial cortex has been implicated in processing sensory information and spatial learning, with abnormal neural activity reported in association with psychedelics and in mouse and non-human primate models of autism spectrum disorders (ASDs). The direct role of the retrosplenial cortex in regulating social behaviors remains unclear. In this work, we reveal that neural activity in the retrosplenial agranular cortex (RSA), a subregion of the retrosplenial cortex, is initially activated, then quickly suppressed upon social contact. This up-down phase of RSA neurons is crucial for normal social behaviors. Parvalbumin-positive GABAergic neurons in the hippocampal CA1 region were found to send inhibitory projections to the RSA. Blocking these CA1-RSA inhibitory inputs significantly impaired social behavior. Notably, enhancing the CA1-RSA inhibitory input rescued the social behavior defects in an ASD mouse model. This work suggests a neural mechanism for the salience processing of social behavior and identifies a potential target for ASD intervention using neural modulation approaches.

中文翻译：

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海马 CA1 到压后无颗粒皮层的抑制性输入对社会行为的门控

摘要

压后皮层与处理感觉信息和空间学习有关，据报道，神经活动异常与迷幻药以及自闭症谱系障碍（ASD）的小鼠和非人类灵长类动物模型有关。压后皮质在调节社会行为中的直接作用仍不清楚。在这项工作中，我们揭示了压后无颗粒皮质（RSA）（压后皮质的一个子区域）中的神经活动最初被激活，然后在社会接触时迅速被抑制。RSA 神经元的这种上下阶段对于正常的社交行为至关重要。研究发现海马 CA1 区小清蛋白阳性 GABA 能神经元向 RSA 发送抑制性投射。阻断这些 CA1-RSA 抑制输入会显着损害社会行为。值得注意的是，增强 CA1-RSA 抑制输入可以挽救 ASD 小鼠模型的社交行为缺陷。这项工作提出了一种用于社会行为显着性处理的神经机制，并使用神经调制方法确定了 ASD 干预的潜在目标。