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

确定血清素和多巴胺转运体结合的变化，这是各自神经元系统的高度选择性标记。使用正电子发射断层扫描，我们分别测量了每个个体的脑血清素和多巴胺转运体与放射性配体碳[11C]McN-5652和[11C]WIN-35,428的结合。参与者从社区中招募。20名男性自闭症患者（年龄18-26岁，平均[SD]智商为99.3[18.1]）和20名年龄和智商匹配的对照组。与对照组相比，自闭症个体的血清素转运体结合在整个大脑中显著降低（p < 0.05）。05年,纠正)。具体而言，孤独症患者的前扣带和后扣带皮层的减少与社会认知障碍有关（p < 0.05）。05年,纠正)。重复性和/或强迫行为和兴趣与丘脑中血清素转运体结合的减少之间也存在显著的相关性(P_。05年,纠正)。相比之下，自闭症组眼眶额叶皮层多巴胺转运体结合显著增加（p < 0.05）。05，在体素分析中修正)。在眶额皮质，多巴胺转运体结合与血清素转运体结合呈显著负相关（r=-0.61； P= 0.004）。自闭症患者的大脑在血清素转运体和多巴胺转运体结合上都有异常。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.