Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia |
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| Authors: | Osamu Miyamoto Takehiro Nakamura Shin-ich Yamagami Tetsuro Negi Masaaki Tokuda Hideki Matsui Toshifumi Itano |
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| Institution: | a Department of Biology, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kagawa 761-0793, Japan;b Department of Neurological Surgery, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kagawa 761-0793, Japan;c Department of Basic Sports Medicine, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kagawa 761-0793, Japan;d Department of Physiology, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kagawa 761-0793, Japan;e Department of Physiology, Okayama University Medical School, 2-5-1, Shikata-cho, Okayama 700-0914, Japan |
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| Abstract: | To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-
-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°C×4 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. |
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| Keywords: | Postischemic hypothermia Long term potentiation Hippocampus Immunohistochemistry N-Methyl- sciencedirect
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-aspartate receptor 1 Gerbil |
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