Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (8): 1254-1259.doi: 10.4103/1673-5374.189189

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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.

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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