Viral infection during pregnancy is correlated with increased frequency of neurodevelopmental disorders, and this is studied in mice prenatally subjected to maternal immune activation (MIA). We previously showed that maternal T helper 17 cells promote the development of cortical and behavioural abnormalities in MIA-affected offspring. Here we show that cortical abnormalities are preferentially localized to a region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ). Moreover, activation of pyramidal neurons in this cortical region was sufficient to induce MIA-associated behavioural phenotypes in wild-type animals, whereas reduction in neural activity rescued the behavioural abnormalities in MIA-affected offspring. Sociability and repetitive behavioural phenotypes could be selectively modulated according to the efferent targets of S1DZ. Our work identifies a cortical region primarily, if not exclusively, centred on the S1DZ as the major node of a neural network that mediates behavioural abnormalities observed in offspring exposed to maternal inflammation.

中文翻译：

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逆转暴露于母体炎症的小鼠的行为异常

怀孕期间的病毒感染与神经发育障碍的频率增加有关，这一点在产前接受母体免疫激活 (MIA) 的小鼠中进行了研究。我们之前表明，母体 T 辅助 17 细胞促进受 MIA 影响的后代皮质和行为异常的发展。在这里，我们显示皮质异常优先定位于包含初级躯体感觉皮层 (S1DZ) 的颗粒障碍区的区域。此外，该皮质区域锥体神经元的激活足以在野生型动物中诱导 MIA 相关的行为表型，而神经活动的减少挽救了受 MIA 影响的后代的行为异常。根据 S1DZ 的传出目标，可以选择性地调节社交性和重复行为表型。我们的工作主要（如果不是全部）以 S1DZ 为中心的皮质区域确定为神经网络的主要节点，该神经网络介导在暴露于母体炎症的后代中观察到的行为异常。