Molecular pathological study on the mechanism of epilepsy in familial epileptic dog

Research Project

Project/Area Number	21580373
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Applied veterinary science
Research Institution	Tottori University
Principal Investigator	MORITA Takehito 鳥取大学, 農学部, 准教授 (70273901)
Project Period (FY)	2009 – 2011
Project Status	Completed (Fiscal Year 2011)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	イヌ / 遺伝 / グルタミン酸 / グルタミン酸トランスポーター / てんかん / 脳 / 神経伝達物質 / 遺伝性 / 免疫電子顕微鏡 / 免疫組織化学 / In situ hybridization
Research Abstract	Prior study in this familial epileptic Shetland sheepdog 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 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 post-translational process of GLT-1 synthesis may be affected.