Exploration of new molecular mechanisms for antidepressant actions of electroconvulsive seizure.
Exploration of new molecular mechanisms for antidepressant actions of electroconvulsive seizure.
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DOI：
10.1248/bpb.34.939
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发表时间：
2011-07
影响因子：
2
通讯作者：
E. Segi-Nishida
中科院分区：
文献类型：
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作者：
E. Segi-Nishida
电惊厥发作（ECS）治疗是一种临床证明的抑郁症治疗方法，即使在对化学抗抑郁药耐药的患者中也经常有效。然而，ECS治疗效果的分子机制尚未完全了解。在这里，我回顾研究表明，ECS治疗的分子，细胞和行为的变化，并讨论ECS的功能，抗抑郁作用的行动。在海马，这些变化包括基因诱导，增加成人神经发生，和电生理反应。特别是，血管内皮生长因子（VEGF）在神经发生中的作用进行了讨论。在海马中的其他基因表达变化中，环氧化酶（考克斯）-2（前列腺素类合成的限速酶的诱导型）的作用受到关注。ECS引起的变化，在其他脑区，如前额叶皮层和下丘脑，和ECS引起的行为变化也进行了审查。了解ECS的分子，细胞和行为变化将提供一个新的视角，以寻找新的抗抑郁药设计的潜在目标，这些发现突出。
Electroconvulsive seizure (ECS) therapy is a clinically proven treatment for depression and is often effective even in patients resistant to chemical antidepressants. However, the molecular mechanisms underlying the therapeutic efficacy of ECS are not fully understood. Here, I review studies that show molecular, cellular, and behavioral changes by ECS treatment, and discuss the functions of ECS to underlie the action of antidepressant effects. In hippocampus, these changes cover gene induction, increased adult neurogenesis, and electrophysiological reactivity. Especially, the role of vascular endothelial growth factor (VEGF) in neurogenesis is discussed. Among other gene expression changes in hippocampus, a role of cyclooxygenase (COX)-2, an inducible type of the rate-limiting enzyme of prostanoid synthesis, is focused. ECS-induced changes in other brain regions such as prefrontal cortex and hypothalamus, and ECS-induced behavioral changes are also reviewed. Understanding the molecular, cellular, and behavioral changes by ECS will provide a new view to find potential targets for novel antidepressant design that are highlighted by these findings.