Abstract：
Ketamine is an NMDA (N-methyl-d-aspartate) glutamate receptor antagonist, which has a myriad of dose-dependent pharmacological and behavioral effects, including anesthetic, sedative, amnestic, analgesic, and anti-inflammatory properties. Intriguingly, ketamine at subanesthetic doses displays a relevant profile both in mimicking symptoms of schizophrenia and also as the first fast-acting treatment for depression. Here, we present an overview of the state-of-the-art knowledge about ketamine as an antidepressant as well as a pharmacological model of schizophrenia in animal models and human participants. Ketamine\'s dual effect appears to arise from its mechanism of action involving NMDA receptors, with both immediate and downstream consequences being triggered as a result. Finally, we discuss the feasibility of a unified approach linking the glutamatergic hypothesis of schizophrenia to the promising preclinical and clinical success of ketamine in the treatment of refractory depression.
摘要：
氯胺酮是一种NMDA（N-甲基-D-天冬氨酸）谷氨酸受体拮抗剂，具有无数剂量依赖性的药理和行为效应，包括麻醉剂,镇静剂,健忘,镇痛药,和抗炎特性。有趣的是，亚麻醉剂量的氯胺酮在模仿精神分裂症的症状以及作为抑郁症的第一种速效治疗方面都显示出相关的特征。这里,我们概述了氯胺酮作为抗抑郁药以及精神分裂症的动物模型和人类参与者的药理学模型的最新知识.氯胺酮的双重作用似乎来自其涉及NMDA受体的作用机制，结果触发了直接和下游的后果。最后,我们讨论了将精神分裂症的谷氨酸能假说与氯胺酮治疗难治性抑郁症的临床前和临床成功联系起来的统一方法的可行性。
