The study related to the neurophysical mechanism of high-functioning autism for using the method of neuroimaging and molecular biology

确定5-羟色胺和多巴胺转运蛋白结合的变化，这是其各自神经系统的高度选择性标记物。使用正电子发射断层扫描，我们测量了每个个体的脑5-羟色胺和多巴胺转运体与放射性配体碳[11 C]McN-5652和[11 C]WIN-35，428的结合。参与者从社区招募。20名男性（年龄范围，18-26岁;平均[SD] IQ，99.3 [18.1]）自闭症患者和20名年龄和IQ匹配的对照受试者。与对照组相比，孤独症患者全脑的5-羟色胺转运体结合率显著降低（P_0.05，校正）。具体而言，前扣带皮层和后扣带皮层的减少与自闭症受试者的社会认知障碍相关（P_0.05，校正）。在重复性和/或强迫性行为和兴趣与丘脑中5-羟色胺转运体结合的减少之间也发现了显著的相关性（P_0.05，校正）。相比之下，自闭症组的眶额皮质中多巴胺转运蛋白结合显著更高（P_0.05，在体素分析中校正）。在眶额皮质，多巴胺转运蛋白结合与5-羟色胺转运蛋白结合呈显著负相关（r=-0.61 ; P=.004）。孤独症患者的大脑在5-羟色胺转运体和多巴胺转运体结合方面都有异常。目前的研究结果表明，这些神经递质系统的严重异常可能是自闭症的神经生理机制的基础。

To determine the occurrence of changes in the binding of serotonin and dopamine transporters, which are highly selective markers for their respective neuronal systems. Using positron emission tomography, we measured the binding of brain serotonin and dopamine transporters in each individual with the radioligands carbon [11C]McN-5652 and [11C]WIN-35,428, respectively. Participants recruited from the community. Twenty men (age range, 18-26 years ; mean [SD] IQ, 99.3 [18.1]) with autism and 20 age- and IQ matched control subjects. Serotonin transporter binding was significantly lower throughout the brain in autistic individuals compared with controls (P_.05, corrected). Specifically, the reduction in the anterior and posterior cingulated cortices was associated with the impairment of social cognition in the autistic subjects (P_.05, corrected). A significant correlation was also found between repetitive and/or obsessive behavior and interests and the reduction of serotonin transporter binding in the thalamus (P_.05, corrected). In contrast, the dopamine transporter binding was significantly higher in the orbitofrontal cortex of the autistic group (P_.05, corrected in voxelwise analysis). In the orbitofrontal cortex, the dopamine transporter binding was significantly inversely correlated with serotonin transporter binding (r=-0.61 ; P=.004). The brains of autistic individuals have abnormalities in both serotonin transporter and dopamine transporter binding. The present findings indicate that the gross abnormalities in these neurotransmitter systems may underpin the neurophysiologic mechanism of autism.