), 王泓婧 江苏师范大学教育科学学院, 徐州 221116
收稿日期:2019-09-15出版日期:2021-07-15发布日期:2021-05-24通讯作者:王志丹E-mail:zwang19@jsnu.edu.cn基金资助:江苏省高等学校自然科学研究项目资助(19KJB190002);2020年度江苏师范大学研究生科研创新项目(2020 XKT227)The neural mechanisms of developmental motor disorders in children with autism spectrum disorder
WANG Lin, WANG Zhidan(), WANG Hongjing School of Education Science, Jiangsu Normal University, Xuzhou 221116, China
Received:2019-09-15Online:2021-07-15Published:2021-05-24Contact:WANG Zhidan E-mail:zwang19@jsnu.edu.cn摘要/Abstract
摘要： 动作发展障碍(Developmental motor disorders)是孤独症谱系障碍的常见特征。通过系统回顾孤独症儿童动作发展障碍的神经科学研究, 发现γ-氨基丁酸和5-羟色胺浓度的改变及γ-氨基丁酸相关蛋白和Shank蛋白的表达异常不仅会损害中枢神经系统的发育, 而且还能导致突触兴奋性与抑制性失衡, 进而改变孤独症儿童小脑和大脑皮层运动区的功能连接。孤独症儿童小脑、基底神经节和胼胝体结构的改变对全脑的连通性产生了负面影响。神经生化机制和脑结构的异常共同导致了脑功能的异常, 最终造成孤独症儿童的动作发展障碍。此外, 动作发展障碍与孤独症核心症状共同的神经基础主要包括镜像神经元系统紊乱, 丘脑、基底神经节和小脑异常以及SLC7A5和PTEN 基因突变。未来研究需要关注与运动密切相关的其他神经递质, 如乙酰胆碱和多巴胺; 探索动作发展障碍神经网络的动态机制及其形成; 剖析该障碍的神经机制和自闭症核心症状神经机制的相互作用。
图/表 1
图1孤独症儿童动作发展障碍的神经生化机制、脑结构基础和脑功能机制的有机关系
图1孤独症儿童动作发展障碍的神经生化机制、脑结构基础和脑功能机制的有机关系参考文献 110
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