Eltokhi Ahmed, Santuy Andrea, Merchan-Perez Angel, Sprengel Rolf
Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, Tübingen University, D-72076 Tübingen, Germany.
Laboratorio Cajal de Circuitos Corticales, Centro de Tecnología Biomédica, Universidad Politécnica de Madrid, 28223 Madrid, Spain.
Int J Mol Sci. 2020 Dec 23;22(1):59. doi: 10.3390/ijms22010059.
The correlation between dysfunction in the glutamatergic system and neuropsychiatric disorders, including schizophrenia and autism spectrum disorder, is undisputed. Both disorders are associated with molecular and ultrastructural alterations that affect synaptic plasticity and thus the molecular and physiological basis of learning and memory. Altered synaptic plasticity, accompanied by changes in protein synthesis and trafficking of postsynaptic proteins, as well as structural modifications of excitatory synapses, are critically involved in the postnatal development of the mammalian nervous system. In this review, we summarize glutamatergic alterations and ultrastructural changes in synapses in schizophrenia and autism spectrum disorder of genetic or drug-related origin, and briefly comment on the possible reversibility of these neuropsychiatric disorders in the light of findings in regular synaptic physiology.
谷氨酸能系统功能障碍与神经精神疾病（包括精神分裂症和自闭症谱系障碍）之间的关联是毋庸置疑的。这两种疾病都与影响突触可塑性的分子和超微结构改变有关，进而影响学习和记忆的分子及生理基础。突触可塑性改变，伴随着蛋白质合成和突触后蛋白转运的变化，以及兴奋性突触的结构修饰，在哺乳动物神经系统的产后发育中起着关键作用。在本综述中，我们总结了精神分裂症和自闭症谱系障碍中遗传或药物相关起源的突触谷氨酸能改变和超微结构变化，并根据正常突触生理学的研究结果简要评论了这些神经精神疾病可能的可逆性。
