The striatum comprises a mosaic structure of striosomal and matrix compartments. Imbalanced neuronal activity between striosomes and matrix is implicated in neurological deficits in psychomotor and limbic functions. Because patients with autism spectrum disorder (ASD) are impaired in social communication and psychomotor function, it raises the possibility that abnormal striatal compartments may contribute to ASD pathogenesis. Here, we provide pathological evidence from human postmortem brains to support this hypothesis. Because ASD is a neurodevelopmental disease that emerges early in childhood, we analyzed juvenile and adolescent brains. Distinct patterns of PRODYNORPHIN-positive and calbindin-poor striosomes were detected in the caudate nucleus of control brains by in situ hybridization and immunohistochemistry. By contrast, PRODYNORPHIN-positive and calbindin-poor striosomes were decreased in the caudate nucleus of young ASD brains. Moreover, calbindin, a matrix marker, was aberrantly increased in the striosomal compartment, obscuring the boundaries between calbindin-poor striosomes and calbindin-rich matrix in ASD caudate nucleus. Calbindin-positive cells were decreased in the ASD matrix compartment. Collectively, our study has uncovered for the first time that aberrant striatal compartments occur in the caudate nucleus of human ASD brains, which suggests abnormal striatal compartmentation as a pathological signature that has previously been underestimated in ASD pathogenesis.

中文翻译：

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自闭症谱系障碍的人脑纹状体部分的病理改变。

纹状体包括纹状体和基质隔室的镶嵌结构。核糖体和基质之间的神经元活动失衡与精神运动和边缘功能的神经功能缺损有关。由于自闭症谱系障碍（ASD）患者的社交和心理运动功能受损，因此增加了异常纹状体隔室可能导致ASD发病的可能性。在这里，我们提供了来自人类死后大脑的病理学证据以支持这一假设。由于ASD是一种在儿童早期出现的神经发育疾病，因此我们分析了青少年和青少年的大脑。通过原位杂交和免疫组织化学在对照组大脑的尾状核中检测到了PRODYNORPHIN阳性和钙结合蛋白差的核糖体的不同模式。相比之下，在年轻的ASD大脑的尾状核中，前强啡肽阳性和钙结合蛋白差的核小体减少。此外，钙结合蛋白，一种基质标志物，在纹状体区室中异常增加，遮盖了贫钙结合蛋白的核小体和富含钙结合蛋白的基质在ASD尾状核之间的边界。在ASD基质区室中钙结合蛋白阳性细胞减少。总的来说，我们的研究首次发现人ASD大脑的尾状核中出现异常的纹状体隔室，这提示异常的纹状体隔室是一种病理学特征，以前在ASD发病机理中被低估了。掩盖ASD尾状核中钙结合蛋白少的质体与富含钙结合蛋白的基质之间的边界。在ASD基质区室中钙结合蛋白阳性细胞减少。总的来说，我们的研究首次发现人ASD大脑的尾状核中出现异常的纹状体隔室，这提示异常的纹状体隔室是一种病理学特征，以前在ASD发病机理中被低估了。掩盖ASD尾状核中钙结合蛋白缺乏的质体与富含钙结合蛋白的基质之间的边界。在ASD基质区室中钙结合蛋白阳性细胞减少。总的来说，我们的研究首次发现人ASD大脑的尾状核中出现异常的纹状体隔室，这提示异常的纹状体隔室是一种病理学特征，以前在ASD发病机理中被低估了。