Abstract：
Electroconvulsive shocks (ECS) and ketamine are antidepressant treatments with a relatively fast onset of therapeutic effects compared to conventional medication and psychotherapy. While the exact neurobiological mechanisms underlying the antidepressant response of ECS and ketamine are unknown, both interventions are associated with neuroplasticity. Restoration of neuroplasticity may be a shared mechanism underlying the antidepressant efficacy of these interventions. In this systematic review, literature of animal models of depression is summarized to examine the possible role of neuroplasticity in ECS and ketamine on a molecular, neuronal, synaptic and functional level, and specifically to what extent these mechanisms are shared between both interventions. The results highlight that hippocampal neurogenesis and brain-derived neurotrophic factor (BDNF) levels are consistently increased after ECS and ketamine. Moreover, both interventions positively affect glutamatergic neurotransmission, astrocyte and neuronal morphology, synaptic density, vasculature and functional plasticity. However, a small number of studies investigated these processes after ECS. Understanding the shared fundamental mechanisms of fast-acting antidepressants can contribute to the development of novel therapeutic approaches for patients with severe depression.
摘要：
电惊厥性休克（ECS）和氯胺酮是抗抑郁治疗，与常规药物和心理治疗相比，治疗效果相对较快。虽然ECS和氯胺酮抗抑郁反应的确切神经生物学机制尚不清楚，两种干预措施都与神经可塑性相关.神经可塑性的恢复可能是这些干预措施抗抑郁功效的共同机制。在这次系统审查中，对抑郁症动物模型的文献进行了总结，以检查ECS和氯胺酮对分子的神经可塑性的可能作用，神经元，突触和功能水平，以及具体到什么程度这些机制是在两种干预措施之间共享。结果强调，ECS和氯胺酮后海马神经发生和脑源性神经营养因子（BDNF）水平持续增加。此外，两种干预措施都对谷氨酸能神经传递产生积极影响，星形胶质细胞和神经元形态学，突触密度,血管和功能可塑性。然而,少数研究调查了ECS后的这些过程。了解快速作用抗抑郁药的共同基本机制可以有助于开发针对重度抑郁症患者的新型治疗方法。
