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中枢5-羟色胺缺乏小鼠成年海马新生神经元树突形态发生增强。

Enhanced dendritic morphogenesis of adult hippocampal newborn neurons in central 5-HT-deficient mice.

作者信息

Song Ning-Ning, Zhang Qiong, Huang Ying, Chen Ling, Ding Yu-Qiang, Zhang Lei

机构信息

Key Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China; Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.

Key Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China; Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.

出版信息

Stem Cell Res. 2017 Mar;19:6-11. doi: 10.1016/j.scr.2016.12.018. Epub 2016 Dec 15.

Abstract

Serotonin (5-HT) plays an important role in regulating adult hippocampal neurogenesis. Chronic administration of selective 5-HT reuptake inhibitors (SSRIs), which up-regulates extracellular 5-HT concentration, accelerates the maturation of adult-born hippocampal neurons. It is unknown, however, about effects of central 5-HT-deficiency on the dendritic morphogenesis of these newborn neurons. Here, we address this question using two central 5-HT-deficient mouse models, Tph2 conditional knockout mice (CKO) losing central 5-HT from embryonic stage, and Pet1-Cre;Rosa26-DTR (diphtheria toxin receptor) mice lacking central 5-HT neurons exclusively in adulthood. The dendritic length of hippocampal newborn neurons is dramatically increased in these mice. Our findings indicate that reducing central 5-HT can accelerate the dendritic maturation of adult-born neurons, thus revealing a new role of central 5-HT in regulating adult hippocampal neurogenesis.

摘要

血清素(5-羟色胺,5-HT)在调节成体海马神经发生中起重要作用。长期给予选择性5-羟色胺再摄取抑制剂(SSRIs)可上调细胞外5-羟色胺浓度,加速成年海马新生神经元的成熟。然而,中枢5-羟色胺缺乏对这些新生神经元树突形态发生的影响尚不清楚。在此,我们使用两种中枢5-羟色胺缺乏的小鼠模型来解决这个问题,即从胚胎期开始就失去中枢5-羟色胺的Tph2条件性敲除小鼠(CKO),以及仅在成年期缺乏中枢5-羟色胺神经元的Pet1-Cre;Rosa26-DTR(白喉毒素受体)小鼠。在这些小鼠中,海马新生神经元的树突长度显著增加。我们的研究结果表明,降低中枢5-羟色胺可加速成年新生神经元的树突成熟,从而揭示了中枢5-羟色胺在调节成体海马神经发生中的新作用。

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