1994 Fiscal Year Final Research Report Summary
Increase in intracellular Ca^<2+> and neuronal injury
Project/Area Number |
04670874
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Cerebral neurosurgery
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Research Institution | Juntendo University |
Principal Investigator |
ARAI Hajime Juntendo Univ. Medical Department Associate Professor, 医学部, 助教授 (70167229)
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Co-Investigator(Kenkyū-buntansha) |
KDOTA Yoshiaki Juntendo Univ. Medical Department Assistant, 医学部, 助手 (60204517)
UDO Akira Juntendo Univ. Medical Department Assistant, 医学部, 助手 (10185051)
YASUMOTO Yukimasa Juntendo Univ. Medical Department Assistant, 医学部, 助手 (20175649)
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Project Period (FY) |
1992 – 1994
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Keywords | Hippocampus / Neuron / Glutamate / Calcium / Cell death / Hypothermia |
Research Abstract |
To elucidate the precise mechanism of neuronal protection by brain hypothermia, we conducted an investigation as to what effect low temperature had on glutamate-induced intracellular free calcium ([Ca^<2+>]i) accumulation and cell death in cultured hippocampal neurons. Fifteen minutes of exposure to either 100muM or 1mM glutamate uniformly induced a marked increase in [Ca^<2+>]i, with delayd recovery and massive neuronal death under the conditions of both 37゚C and 30゚C.The study indicated that brain hypothermia cannot save neurons once glutamate is released during ischemia, and that intraischemic hypothermia in vivo probably prevents the development of ischemic neuronal injuly by suppressing extracellular glutamate release.
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