Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia

Osamu Miyamoto, Takehiro Nakamura, Shin ich Yamagami, Tetsuro Negi, Masaaki Tokuda, Hideki Matsui, Toshifumi Itano

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)168-172
Number of pages5
JournalBrain Research
Issue number1
Publication statusPublished - Aug 4 2000


  • Gerbil
  • Hippocampus
  • Immunohistochemistry
  • Long term potentiation
  • N-Methyl-D-aspartate receptor 1
  • Postischemic hypothermia

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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