谷氨酸假说（与神经可塑性假说有关） *谷氨酸系统功能障碍导致大脑中负责抑郁症状表达的区域发生结构性、适应性的变化 *谷氨酰胺能传递的药理学调节剂导致BDNF的表达，产生与抗抑郁相关的突触/细胞可塑性变化 *大脑中谷氨酸能传递的调节可以触发快速抗抑郁反应的机制 Figure 2:Glutamatergic targets with potential antidepressant effects NMDA antagonists: ketamine.CP-101.606.AZD6765. Ro25-6981.GLYX-13 mGluR2/3 antagonists: Muscarinic antagonists: LY341495 scopolamine, Spine synapse MGS0039 telenzapine number and NMDA function MuscR Glutamate mGluR2/3 GABA Glutamate AMPA potentiating Glutamate burst ↑BDNF release agents AMPA罪NMDA 4 AMPA GSK3 Depression relapse GSK PP GSK3 antagonists: lithium or mTOR selective inhibitor SB216763 Rapamycin Akt protein kinase B;AMPA =a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid;BDNF=brain-derived neurotrophic factor;ERK extracellular signal-regulated kinases;GABA gamma-aminobutyric acid;GSK=glycogen synthase kinase;mGlu2/3=metabotropic glutamate receptor 2/3;mTOR=mammalian target of rapamycin;MuscR muscarinic receptor;NMDA =N-methyl-D-aspartate;PP1=protein phosphatase 1;TrkB =tropomyosin receptor kinase B* 谷氨酸系统功能障碍导致大脑中负责抑郁症状表达的区域发生结构性、适应性的变化 * 谷氨酰胺能传递的药理学调节剂导致BDNF的表达，产生与抗抑郁相关的突触/细胞可塑性变化 * 大脑中谷氨酸能传递的调节可以触发快速抗抑郁反应的机制 谷氨酸假说（与神经可塑性假说有关）