Induction of Neuron-derived Orphan Receptor-1 in the Dentate Gyrus of the Hippocampal Formation Following Transient Global Ischemia in the Rat

  • Kim, Younghwa (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Hong, Soontaek (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Noh, Mi Ra (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Kim, Soo Young (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Huh, Pil Woo (Department of Neurosurgery, Uijongbu St. Mary's Hospital, Catholic University,) ;
  • Park, Sun-Hwa (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Sun, Woong (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University) ;
  • Kim, Hyun (Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University)
  • Received : 2005.12.12
  • Accepted : 2006.05.22
  • Published : 2006.08.31

Abstract

Neuron-derived orphan receptor (NOR-1) is a member of the thyroid/steroid receptor superfamily that was originally identified in forebrain neuronal cells undergoing apoptosis. In addition to apoptotic stimuli, activation of several signal transduction pathways including direct neuronal depolarization regulates the expression of NOR-1. In this study we tested whether the expression of NOR-1 is changed following transient ischemic injury in the adult rat brain. NOR-1 mRNA increased rapidly in the dentate gyrus of the hippocampal formation and piriform cortex 3 h after transient global ischemia and returned to basal level at 6 h. On the other hand, oxygen-glucose deprivation of cultured cerebral cortical neurons did not alter the expression of NOR-1. These results suggest that expression of NOR-1 is differentially regulated in different brain regions in response to globally applied brain ischemia, but that hypoxia is not sufficient to induce its expression.

Keywords

Acknowledgement

Supported by : Korean Ministry of Health and Welfare, Korea Science and Engineering Foundation

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