Chronic stress (CS) is associated with a number of neuropsychiatric disorders, and it may also contribute to or exacerbate motor function. However, the mechanisms by which stress triggers motor symptoms are not fully understood. Here, we report that CS functionally alters dorsomedial striatum (DMS) circuits in male mice, by affecting GABAergic interneuron populations and somatostatin positive (SOM) interneurons in particular. Specifically, we show that CS impairs communication between SOM interneurons and medium spiny neurons, promoting striatal overactivation/disinhibition and increased motor output. Using probabilistic machine learning to analyze animal behavior, we demonstrate that in vivo chemogenetic manipulation of SOM interneurons in DMS modulates motor phenotypes in stressed mice. Altogether, we propose a causal link between dysfunction of striatal SOM interneurons and motor symptoms in models of chronic stress.

慢性应激 (CS) 与许多神经精神疾病有关，它也可能促进或加剧运动功能。然而，压力引发运动症状的机制尚不完全清楚。在这里，我们报告 CS 通过影响 GABAergic 中间神经元群体和特别是生长抑素阳性 (SOM) 中间神经元，在功能上改变雄性小鼠的背内侧纹状体 (DMS) 回路。具体来说，我们表明 CS 会损害 SOM 中间神经元和中型多刺神经元之间的交流，促进纹状体过度激活/去抑制和增加运动输出。使用概率机器学习来分析动物行为，我们证明了 DMS 中 SOM 中间神经元的体内化学遗传操作可调节应激小鼠的运动表型。共，