Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants
Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants
复制标题
DOI：
10.1126/science.1083328
复制
发表时间：
2003-08-08
期刊：
影响因子：
56.9
通讯作者：
Hen, R
中科院分区：
文献类型：
--
作者：
Santarelli, L;Saxe, M;Hen, R
各种慢性抗抑郁治疗增加成年海马神经发生，但这种现象的功能重要性尚不清楚。在这里，使用遗传学和放射学方法，我们表明，破坏抗抑郁药诱导的神经发生阻断抗抑郁药的行为反应。5-羟色胺1A受体缺失小鼠对氟西汀（一种5-羟色胺选择性再摄取抑制剂）的神经和行为效应不敏感。X射线照射小鼠大脑中含有海马的限制区域可以防止两类抗抑郁药的神经和行为效应。这些发现表明，慢性抗抑郁药的行为效应可能是通过刺激海马神经发生介导的。
Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.