| Project/Area Number |
11557035
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Legal medicine
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKASONO Ichiro Nagasaki University, Legal Medicine, Professor, 医学部, 教授 (30108287)
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| Co-Investigator(Kenkyū-buntansha) |
ORIHARA Yoshiyuki Nagasaki University, Legal Medicine, Lecture, 医学部, 講師 (70264215)
TSUDA Ryouichi Nagasaki University, Legal Medicine, Lecture, 医学部, 講師 (20098875)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥11,800,000 (Direct Cost: ¥11,800,000)
Fiscal Year 2000: ¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1999: ¥6,800,000 (Direct Cost: ¥6,800,000)
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| Keywords | Glutamate / Transporter / Human / Neurotranmitter / Excitatory Amino Acid / 法医剖検脳 / グルタミン酸トランスポーター / アストロサイト / 免疫組織化学 |
|---|
| Research Abstract |
Glutamate is the major excitatory neurotransmitter and the greater part of this amino acid is removed from the synaptic cleft by excitatory amino acid transporter 2 (EAAT2) located on perisynaptic astrocytes. Recently, it was reported that the EAAT2 protein content changed in rats following forebrain ischemia and administration of methamphetamine. We planned to demonstrate the immunohistochemical distribution of EAAT2 in the human brain and discuss the significance of its pathophysiological roles. Thirty-eight cases were used from forensic autopsies. The tissues were sampled from the cerebral cortex, striatum and hippocampus. The distribution of EAAT2 was difficult to identify in cases of electrical fatalities. However, continuous and extensive staining of EAAT2 was observed in cases of death from hypothermia. In almost all asphyxia death, we were able to observe a weak stain of EAAT2. In case of solvent abuse, EAAT2 staining was continuous and extensive as in the cases of hypothermia, and patchy negative zones were mixed. This study clearly showed the differences in EAAT2 localization according to the cause of death. These findings suggested that the differences in EAAT2 staining depended on the cause and course (pathophysiological conditions) of death.
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