Suppr超能文献

实验性中风后氟西汀的神经可塑性及行为学效应

Neuroplasticity and behavioral effects of fluoxetine after experimental stroke.

作者信息

Sun Yefei, Sun Xiaoyu, Qu Huiling, Zhao Shanshan, Xiao Ting, Zhao Chuansheng

机构信息

Gastrointestinal Surgery, The First Hospital of China Medical University, Shenyang, China.

Department of Neurology, The People's Hospital of Liaoning Province, Shenyang, China.

出版信息

Restor Neurol Neurosci. 2017;35(5):457-468. doi: 10.3233/RNN-170725.

Abstract

The brain can undergo self-repair and has the ability to compensate for functions lost after a stroke. The plasticity of the ischemic brain is influenced by several factors including aging and pharmacotherapy. Fluoxetine is an antidepressant which enhances serotonergic neurotransmission through selective inhibition of neuronal reuptake of serotonin. In clinical practice, fluoxetine alleviates the symptoms of post-stroke depression (PSD), helps motor recovery in stroke patients. In animal experiments, chronic administration of fluoxetine induces increased excitability of mature granule cells (GCs), enhancing axonal and dendritic reorganization, as well as promoting neurogenesis or angiogenesis in the dentate gurus (DG), but the effect of fluoxetine in the subventricular zone (SVZ) remains controversial. Meanwhile, chronic treatment with fluoxetine did not reverse age-dependent suppression of proliferation cells in the DG. Interestingly, although fluoxetine has been found to enhance neurogenesis in the DG in stroke rats, this property is not consistent with the behavioral recovery. More studies into this issue will be required to reveal how to translate enhanced neuronal plasticity into behavioral benefits. This review provides an update of the current knowledge about the neurogenesis and the fate of the newly generated cells after the use of fluoxetine, as well as its ability to promote a behavioral recovery after stroke in clinical and experimental results and attempts to define the therapeutic properties of fluoxetine in regenerative neuroscience.

摘要

大脑能够进行自我修复,并具有补偿中风后丧失功能的能力。缺血性脑的可塑性受包括衰老和药物治疗在内的多种因素影响。氟西汀是一种抗抑郁药,它通过选择性抑制神经元对5-羟色胺的再摄取来增强5-羟色胺能神经传递。在临床实践中,氟西汀可缓解中风后抑郁(PSD)的症状,有助于中风患者的运动恢复。在动物实验中,长期给予氟西汀可诱导成熟颗粒细胞(GCs)兴奋性增加,增强轴突和树突的重组,并促进齿状回(DG)中的神经发生或血管生成,但氟西汀在脑室下区(SVZ)的作用仍存在争议。同时,氟西汀的长期治疗并未逆转DG中与年龄相关的增殖细胞抑制。有趣的是,尽管已发现氟西汀可增强中风大鼠DG中的神经发生,但这种特性与行为恢复并不一致。需要对这个问题进行更多研究,以揭示如何将增强的神经元可塑性转化为行为益处。本综述提供了关于使用氟西汀后神经发生和新生成细胞命运的当前知识更新,以及其在临床和实验结果中促进中风后行为恢复的能力,并试图确定氟西汀在再生神经科学中的治疗特性。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验