Prenatal stress (PS) can impact fetal brain structure and function and contribute to higher vulnerability to neurodevelopmental and neuropsychiatric disorders. To understand how PS alters evoked and spontaneous neocortical activity and intrinsic brain functional connectivity, mesoscale voltage imaging was performed in adult C57BL/6NJ mice that had been exposed to auditory stress on gestational days 12–16, the age at which neocortex is developing. PS mice had a four-fold higher basal corticosterone level and reduced amplitude of cortical sensory-evoked responses to visual, auditory, whisker, forelimb, and hindlimb stimuli. Relative to control animals, PS led to a general reduction of resting-state functional connectivity, as well as reduced inter-modular connectivity, enhanced intra-modular connectivity, and altered frequency of auditory and forelimb spontaneous sensory motifs. These resting-state changes resulted in a cortical connectivity pattern featuring disjoint but tight modules and a decline in network efficiency. The findings demonstrate that cortical connectivity is sensitive to PS and exposed offspring may be at risk for adult stress-related neuropsychiatric disorders.

产前压力（PS）会影响胎儿的大脑结构和功能，并导致更容易出现神经发育和神经精神疾病。为了了解 PS 如何改变诱发和自发的新皮质活动以及内在的大脑功能连接，对在妊娠第 12-16 天（新皮质正在发育的年龄）暴露于听觉压力的成年 C57BL/6NJ 小鼠进行了中尺度电压成像。 PS 小鼠的基础皮质酮水平高出四倍，并且对视觉、听觉、胡须、前肢和后肢刺激的皮质感觉诱发反应幅度降低。相对于对照动物，PS导致静息态功能连接性普遍减少，以及模块间连接性减少、模块内连接性增强以及听觉和前肢自发感觉基序的频率改变。这些静息状态的变化导致了皮质连接模式的特征是不相交但紧密的模块和网络效率的下降。研究结果表明，皮质连接对 PS 敏感，暴露于 PS 的后代可能面临成人压力相关神经精神疾病的风险。