Anatomy: Transient increases of glutamic acid decarboxylase 67 immunoreactivity and its protein levels in the somatosensory cortex after transient cerebral ischemia in gerbils

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  • HWANG In Koo
    Department of Anatomy and Cell Biology, College of Veterinary Medicine and BK21 Program for Veterinary Science, Seoul National University
  • YOO Ki-Yeon
    Department of Anatomy and Neurobiology, College of Medicine, Hallym University
  • LI Hua
    Department of Anatomy and Neurobiology, College of Medicine, Hallym University
  • PARK Ok Kyu
    Department of Anatomy and Neurobiology, College of Medicine, Hallym University
  • LEE Choong Hyun
    Department of Anatomy and Cell Biology, College of Veterinary Medicine and BK21 Program for Veterinary Science, Seoul National University
  • CHOI Jung Hoon
    Department of Anatomy and Neurobiology, College of Medicine, Hallym University
  • KWON Dae Young
    Korea Food Research Institute
  • WON Moo-Ho
    Department of Anatomy and Neurobiology, College of Medicine, Hallym University Institute of Neurodegeneration and Neuroregeneration, Hallym University

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  • Transient Increases of Glutamic Acid Decarboxylase 67 Immunoreactivity and Its Protein Levels in the Somatosensory Cortex after Transient Cerebral Ischemia in Gerbils

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説明

In this study, we investigated changes in glutamic acid decarboxylase 67 (GAD67) immunoreactivity and its protein levels in the gerbil somatosensory cortex after ischemia/reperfusion. GAD67 immunoreactivity was significantly increased in layers III and V of the somatosensory cortex 12 hr after ischemia/reperfusion. Thereafter, GAD67 immunoreactivity was decreased with time after ischemia/reperfusion. GAD67 immunoreactivity in the somatosensory cortex 4 days after ischemia/reperfusion was similar to that in the sham-operated group. In addition, GAD67 protein levels were also significantly increased 12 hr after transient forebrain ischemia. These results suggest that the transient increase of GAD67 immunoreactivity in layers III and V may be associated with responses to transient ischemia-induced neuronal damage.<br>

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