Takeuchi Yoshihiro
Department of Pediatrics, Shiga University of Medical Science, Otsu, Shiga.
No To Hattatsu. 2008 Nov;40(6):451-5.
Attention deficit/hyperactivity disorder (AD/HD) is a heterogeneous developmental disorder with an etiology that is not fully understood. AD/HD has been considered to occur due to a disturbance in cathecholaminergic neurotransmission, with particular emphasis on dopamine. The neurotransmission of dopamine in subcortical regions such as the basal ganglia and limbic areas is synaptic; on the other hand, dopamine neurotransmission in the frontal cortex is quite different, because there are very few dopamine transporters (DAT) in the frontal cortex that allow dopamine to diffuse away from the dopamine synapse ("volume transmission"). It is now clear that noradrenergic neurons play a key regulatory role in dopaminergic function in the frontal cortex. Furthermore, serotonergic neurons exert an inhibitory effect on midbrain dopamine cell bodies, and they have an influence on dopamine release in terminal regions. There is accumulating neurobiological evidence pointing toward a role of the serotonin system in AD/HD. The etiology of autism spectrum disorders (ASD) is still unclear, but information from genetics, neuropathology, brain imaging, and basic neuroscience has provided insights into the understanding of this developmental disorder. In addition to abnormal circuitry in specific limbic and neocortical areas of the cerebral cortex, impairments in brainstem, cerebellar, thalamic, and basal ganglia connections have been reported. Numerous studies have pointed to abnormalities in serotonin and glutamate neurotransmission. Three important aspects involved in the pathophysiology of ASD have been proposed. The first is cell migration, the second is unbalanced excitatory-inhibitory networks, and the third is synapse formation and pruning, the key factors being reelin, neurexin, and neuroligin. Serotonin is considered to play an important role in all of these aspects of the pathophysiology of ASD. Finally, I would like to emphasize that it is crucial in the field of child neurology medical examination and treatment should be based on the basic neuroscience, always taking "neurons" into consideration.
注意力缺陷/多动障碍(AD/HD)是一种病因尚未完全明确的异质性发育障碍。AD/HD被认为是由于儿茶酚胺能神经传递紊乱所致,尤其侧重于多巴胺。多巴胺在基底神经节和边缘区域等皮质下区域的神经传递是通过突触进行的;另一方面,额叶皮质中的多巴胺神经传递则大不相同,因为额叶皮质中多巴胺转运体(DAT)极少,这使得多巴胺能够从多巴胺突触扩散开来(“容积传递”)。现在已经明确,去甲肾上腺素能神经元在额叶皮质的多巴胺功能中起着关键的调节作用。此外,5-羟色胺能神经元对中脑多巴胺细胞体发挥抑制作用,并对终末区域的多巴胺释放产生影响。越来越多的神经生物学证据表明5-羟色胺系统在AD/HD中发挥作用。自闭症谱系障碍(ASD)的病因仍不明确,但来自遗传学、神经病理学、脑成像和基础神经科学的信息为理解这种发育障碍提供了线索。除了大脑皮质特定边缘和新皮质区域的异常神经回路外,还报告了脑干、小脑、丘脑和基底神经节连接的损伤。众多研究指出5-羟色胺和谷氨酸神经传递存在异常。有人提出了ASD病理生理学涉及的三个重要方面。第一个是细胞迁移,第二个是兴奋性-抑制性网络失衡,第三个是突触形成和修剪,关键因素是Reelin、神经纤连蛋白和神经连接蛋白。5-羟色胺被认为在ASD病理生理学所有这些方面都发挥着重要作用。最后,我想强调的是,在儿童神经病学领域,至关重要的是医疗检查和治疗应基于基础神经科学,始终要考虑到“神经元”。