中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (8): 1254-1259.doi: 10.4103/1673-5374.189189

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

短暂性前脑缺血沙鼠海马的葡萄糖代谢及神经发生

  

  • 出版日期:2016-08-31 发布日期:2016-08-31
  • 基金资助:
    韩国教育部基础科学研究项目;韩国Kangwon国立大学2013研究项目;韩国首尔国立大学兽医科学研究所资助项目

Glucose metabolism and neurogenesis in the gerbil hippocampus after transient forebrain ischemia

Dae Young Yoo1, #, Kwon Young Lee2, #, Joon Ha Park3, Hyo Young Jung1, Jong Whi Kim1, Yeo Sung Yoon1, Moo-Ho Won3, Jung Hoon Choi2, *, In Koo Hwang1, *   

  1. 1 Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, South Korea 2 Department of Anatomy, College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University, Chuncheon, South Korea 3 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea
  • Online:2016-08-31 Published:2016-08-31
  • Contact: Jung Hoon Choi, D.V.M., Ph.D., or In Koo Hwang, D.V.M, Ph.D., jhchoi@kangwon.ac.kr or vetmed2@snu.ac.kr
  • Supported by:
    This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, No. NRF-2013R1A1A2059364, NRF-2015R1D1A3A01020635); by 2013 Research Grant from Kangwon National University, and also partially supported by the Research Institute for Veterinary Science, Seoul National University.

摘要:

近年研究表明,在脑的能量代谢中葡萄糖转运体3(GLUT3)中发挥着重要作用。以往研究主要为局灶性或缺氧缺血性动物模型GLUT3mRNA和蛋白表达的变化,而对短暂性前脑缺血组织水平的GLUT3变化则未见报道。实验观察了短暂性前脑缺血5min成年沙鼠海马GLUT3免疫反应的随时间变化。发现假手术组沙鼠海马CA1区GLUT3免疫反应很弱。沙鼠脑缺血后24h海马CA1区锥体细胞GLUT3免疫反应随时间延长而逐渐加强;缺血后2-5d,海马CA1区GLUT3免疫反应明显下降。GLUT3/胶质纤维酸性蛋白(GFAP)免疫荧光双标检测显示,缺血海马CA1区GLUT3免疫反应主要存在于星形胶质细胞中;GLUT3/双皮质素(DCX)免疫荧光双标检测显示,缺血海马GLUT3免疫反应主要存在于齿状回颗粒下层分化的成神经细胞中。假手术组沙鼠GLUT3免疫反应主要存在于海马齿状回颗粒下层。这些结果表明,GLUT3在海马CA1区的变化可能代偿性起到调节葡萄糖水平的作用,并促进齿状回神经发生。 

orcid: 0000-0002-3725-4907 (Jung Hoon Choi) 0000-0002-0533-4638 (In Koo Hwang)

关键词: 神经再生, 短暂性脑缺血, 葡萄糖转运体3, 锥体细胞, 星形胶质细胞, 成神经细胞

Abstract: Recent evidence exists that glucose transporter 3 (GLUT3) plays an important role in the energy metabolism in the brain. Most previous studies have been conducted using focal or hypoxic ischemia models and have focused on changes in GLUT3 expression based on protein and mRNA levels rather than tissue levels. In the present study, we observed change in GLUT3 immunoreactivity in the adult gerbil hippocampus at various time points after 5 minutes of transient forebrain ischemia. In the sham-operated group, GLUT3 immunoreactivity in the hippocampal CA1 region was weak, in the pyramidal cells of the CA1 region increased in a time-dependent fashion 24 hours after ischemia, and in the hippocampal CA1 region decreased signifcantly between 2 and 5 days after ischemia, with high level of GLUT3 immunoreactivity observed in the CA1 region 10 days after ischemia. In a double immuno?uorescence study using GLUT3 and glial-fbrillary acidic protein (GFAP), we observed strong GLUT3 immunoreactivity in the astrocytes. GLUT3 immunoreactivity increased after ischemia and peaked 7 days in the dentate gyrus after ischemia/reperfusion. In a double immuno?uorescence study using GLUT3 and doublecortin (DCX), we observed low level of GLUT3 immunoreactivity in the differentiated neuroblasts of the subgranular zone of the dentate gyrus after ischemia. GLUT3 immunoreactivity in the sham-operated group was mainly detected in the subgranular zone of the dentate gyrus. These results suggest that the increase in GLUT3 immunoreactivity may be a compensatory mechanism to modulate glucose level in the hippocampal CA1 region and to promote adult neurogenesis in the dentate gyrus.

Key words: nerve regeneration, transient forebrain ischemia, glucose transporter 3, pyramidal cells, astrocytes; neuroblasts, neural regeneration