近年临床研究表明,单次注射低剂量谷氨酸N-甲基-D-天门冬氨酸(NMDA)受体拮抗剂氯胺酮可以在2小时内缓解抑郁症状,药效持续长达一周,引发抑郁症治疗领域的高度关注,但氯胺酮的快速起效抗抑郁机制至今尚不明确。最近李楠欣等人研究发现氯胺酮能快速激活哺乳动物的雷帕霉素靶点(mTOR)途径,从而导致大鼠前额皮质突触信号蛋白增多及棘突触数量增加。NMDA受体的其他拮抗剂,如CP-101606(曲索罗地)等也能产生与氯胺酮类似的抗抑郁作用,激活mTOR信号通路。这些研究表明,mTOR信号通路很有可能是一种新型快速起效抗抑郁药治疗的靶点。 In recent years, clinical studies have shown that a single injection of low-dose glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine can relieve depression symptoms within 2 hours, the efficacy lasts up to a week, triggering depression The field of disease treatment is highly concerned, but the mechanism of ketamine's rapid onset of antidepressant effect is still unclear. Recently, Li Nanxin et al. Found that ketamine rapidly activates the mammalian target of rapamycin (mTOR), leading to an increase in rat synaptic signaling proteins and an increase in the number of spines and synapses. Other antagonists of NMDA receptors, such as CP-101606 (trastuzumab), also produce similar antidepressant effects as ketamine, activating the mTOR signaling pathway. These studies suggest that the mTOR signaling pathway is likely to be a novel target for the rapid onset of antidepressant treatment.