Functional lateralization of the prefrontal cortex has been implicated in stress and emotional disorders, yet underlying gene expression changes remains unknown. Here, we report molecular signatures lateralized by chronic social defeats between the two medial prefrontal cortices (mPFCs). Stressed mice show 526 asymmetrically expressed genes between the mPFCs. This cortical asymmetry selectively occurs in stressed mice with depressed social activity, but not in resilient mice with normal behavior. We have isolated highly asymmetric genes including connective tissue growth factor (CTGF), a molecule that modulates wound healing at the periphery. Knockdown of CTGF gene in the right mPFC by shRNA led to a stress-resistant behavioral phenotype. Overexpression of CTGF in the right mPFC using viral transduction induces social avoidance while the left mPFC thereof prevent stress-induced social avoidance. Our study provides a molecular window into the mechanism of stress-induced socioemotional disorders, which can pave the way for new interventions by targeting cortical asymmetry.

中文翻译：

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分子偏侧性编码内侧前额叶皮层的压力敏感性


前额皮质的功能侧化与压力和情绪障碍有关，但潜在的基因表达变化仍然未知。在这里，我们报告了两个内侧前额皮质（mPFC）之间因长期社交失败而侧化的分子特征。应激小鼠的 mPFC 之间显示出 526 个不对称表达的基因。这种皮质不对称选择性地发生在社交活动抑郁的应激小鼠中，但不会发生在行为正常的弹性小鼠中。我们分离出高度不对称的基因，包括结缔组织生长因子（CTGF），这是一种调节外周伤口愈合的分子。 shRNA 敲低右侧 mPFC 中的 CTGF 基因导致了抗应激行为表型。使用病毒转导在右侧mPFC中过度表达CTGF诱导社交回避，而其左侧mPFC防止压力诱导的社交回避。我们的研究为研究压力引起的社会情绪障碍的机制提供了一个分子窗口，这可以为针对皮质不对称的新干预措施铺平道路。