DCX-Expressing Neurons Decrease in the Retrosplenial Cortex after Global Brain Ischemia

  • Nobuo KutsunaEmail author
  • Yoshihiro Murata
  • Takashi Eriguchi
  • Yoshiyuki Takada
  • Hideki Oshima
  • Kaoru Sakatani
  • Yoichi Katayama
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 765)


Many studies have demonstrated cognitive function disorders including space learning disorders after global brain ischemia (GBI). Previous research on space perception and learning has indicated that the retrosplenial cortex (RS) is strongly involved. We performed immunostaining with doublecortin (DCX) for neurons with plasticity potential in the RS and investigated the neuronal numbers to assess the changes of plasticity in the RS following GBI. We employed male Sprague–Dawley rats and carried out bilateral carotid arterial occlusion for 10 min as a GBI model (control, n = 5; GBI model, n = 5). We counted the right and left hemispheres separately on two serial sections, for a total of four regions per animal to examine the differences in expression related to GBI. Additionally, we performed Fluoro-Jade B (FJB) staining to investigate the cause of any DCX-expressing neuron decrease. The total number of DCX-expressing neurons was 1,652 and 912 in the controls and GBI model, respectively. The mean number of DCX-expressing neurons per unit area was significantly lower in the GBI model than in the controls. FJB positive neurons were not found in the RS, while many were present in the ­hippocampus CA1 after GBI. The decrease of DCX-expressing neurons in the RS indicated a plasticity decrease following GBI. The lack of FJB positive neurons in the RS after GBI suggested that the decrease of DCX-expressing neurons in the RS was not due to neuronal cell death in contrast to the hippocampus CA1, while the FJB positive neurons in the hippocampus indicated a delayed neuronal cell death as observed in many previous studies.


Brain ischemia 



This work was supported in part by a Grant-in-Aid for Scientific Research (C-20591725) and by the Strategic Research Program for Brain Science (MEXT), a grant from the Ministry of Education, Culture, Sports, Science and Technology of Japan (C-18591614) and a grant for the promotion of industry–university collaboration at Nihon University.


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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Nobuo Kutsuna
    • 1
    Email author
  • Yoshihiro Murata
    • 1
  • Takashi Eriguchi
    • 1
  • Yoshiyuki Takada
    • 1
  • Hideki Oshima
    • 1
  • Kaoru Sakatani
    • 2
  • Yoichi Katayama
    • 1
  1. 1.Division of Neurosurgery, Department of Neurological SurgeryNihon University School of MedicineTokyoJapan
  2. 2.Division of Optical Brain Engineering, Department of Neurological SurgeryNihon University School of MedicineTokyoJapan

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