Autism is one of the urgent problems in neuroscience. Early research in our laboratory found that dcf1 gene-deficient mice exhibited autistic behavior. Reviewing the literature, we know that the caudate putamen (CPu) brain region is closely related to the occurrence of autism. In this study, we observed that the electrical signal in the abnormal brain region of adult mice was enhanced by using field potential detection for the corresponding brain region. We then used retrovirus markers to track neurons in the CPu brain region and found that there are neural projections in the hippocampus-CPu brain region. Therefore, we selected DREADDs (Designer receptors exclusively activated by designer drugs) to inhibit the abnormal brain region of the mouse and found, through behavioral testing, that this can inhibit the autistic behavior of mice. This research provides new evidence for the understanding of the cause of autism and has accumulated new basis for the treatment of autism. It has theoretical significance and potential application value for the understanding and treatment of autism.

自闭症是神经科学中亟待解决的问题之一。我们实验室的早期研究发现dcf1基因缺陷小鼠表现出自闭症行为。查阅文献可知，尾壳核（CPu）脑区与自闭症的发生密切相关。在本研究中，我们观察到通过对相应脑区进行场电位检测，成年小鼠异常脑区的电信号得到增强。然后我们使用逆转录病毒标记来追踪 CPu 脑区的神经元，发现海马-CPu 脑区存在神经投射。因此，我们选择了 DREADDs（由设计师药物专门激活的设计师受体）来抑制小鼠的异常大脑区域，并通过行为测试发现这可以抑制小鼠的自闭症行为。该研究为认识孤独症的病因提供了新的证据，为孤独症的治疗积累了新的依据。对自闭症的认识和治疗具有理论意义和潜在应用价值。