| Project/Area Number |
12680765
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience |
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Principal Investigator |
OKADA Haruoo Tokyo Metropolitan Organization For Medical Research, Tokyo Metropolitan Institute for Neuroscience, Staff scientist, 東京都神経科学総合研究所, 副参事研究員 (60221842)
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| Co-Investigator(Kenkyū-buntansha) |
KONDO Masahiro Tokyo Metropolitan Organization For Medical Research, Tokyo Metropolitan Institute for Neuroscience, Staff scientist, 東京都神経科学総合研究所, 研究員 (50312294)
MIWA Akiko Tokyo Metropolitan Organization For Medical Research, Tokyo Metropolitan Institute for Neuroscience, Staff scientist, 東京都神経科学総合研究所, 研究員 (60142155)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | AMPA receptor / GIuR1 / GIuR2 / BDNF / adenovirus / Ca2+ permeability / GFP / cultured neuron / 細胞生存 / カルシウム透過性 / Fura-2 |
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| Research Abstract |
(1) In the rat forebrain region, the majority of GluR1-/GluR2-expressing neurons with either calcium-binding proteins (parvalbumin- or calbindm-D28k) corresponded to the GluR1 predominant neurons. By measuring the changes in intracellular calcium concentration, it was resulted that the expression of calcium-binding proteins may correlates with the calcium permeability through AMPA receptors.
(2) After unilateral orbital enucleations in rats within a week after birth, lower expression of GluR2 mRNA was observed in the neurons of the contra lateral side as comp aired with that of the ipsilateral side in SO, but in SGS. These results indicate that GluR2 expression in the SO neurons is regulated by the correct afferentation from the retina.
(3) BDNF enhanced both GluR1 and GluR2 expressions in the rat cortical cultured neurons. To evaluate the expression in individual cell level, GluR1/GluR2 ratio was increased in some cells, while GluR1/GluR2 ratio was reduced in the other cells.
(4) To analyze the dynamic localization of AMPA receptor subunits, we constructed the mycGFP-GluR2, mycGluR2Q and mycYFPGluR1 expressing adenovirus vectors. The results suggested that the calbindin D28k enhanced the GluR2Q expression on the surface of cell membranes.
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