| Project/Area Number |
17580266
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied veterinary science
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| Research Institution | Tottori University |
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Principal Investigator |
MORITA Takehito Tottori University, Faculty of Agriculture, Associate Professor, 農学部, 助教授 (70273901)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | epilepsy / neurotransmitter / glutamate / glutamate transporter / dog / genetic / immunoelectron / In situ hybridization / グルタミン酸トランスポーター |
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| Research Abstract |
Epilepsy is one of the most common and significant disorders of the central nervous system, characterized by recurrent seizures. Recently, some studies suggested that epileptic seizures are associated with down regulation of GLT-1, one of the glutamate transporters, and that the collapse of extracellular glutamate (Glu) regulation caused by a functional failure of GLT-1 may be responsible for epileptogenesis. A familial epileptic Shetland sheepdog colony has been maintained in this laboratory. Prior study has suggested that a decrease of GLT-1 expression in astrocytes in the cortex under the sulcus may be responsible for the occurrence of abnormal electroencephalographic waves in the familial dogs. In this study, we investigated where the process of GLT-1 synthesis would be affected in astrocytes. Immunohistochemically, a decrease of GLT-1 immunolabellings was found in the cerebral cortex under the sulcus. In situ hybridization demonstrated no significant changes of GLT-1 mRNA labellings in the cortex under the sulcus of all familial dogs. In immunoelectron microscopy, GLT-1 immunolabellings were detected in endoplasmic reticulum (ER), while not the plasma membrane of astrocytes in the familial cortex under the sulcus. These results suggested at least two possibilities that GLT-1 synthesis process may stop in ER following an incomplete translation, or that the posttranslational process of GLT-1 synthesis were affected.
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