| Project/Area Number |
15500223
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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 |
Neuroscience in general
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| Research Institution | Tokyo Metropolitan Organization for Medical Research |
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Principal Investigator |
OKADO Haruo Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for neuroscience, Staff Sceintist, 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) |
MIWA Akiko Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for neuroscience, Staff Sceintist, 東京都神経科学総合研究所, 研究員 (60142155)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Glutamate receptor / calbindinD28k / AMPA receptor / CREB / calcium binding protein / カルシウム透過型AMPA受容体 / CalbindinD28k / NMDA受容体 / カルシウム結合蛋白 / paravalbumin / AMPA受容体 / カルビンジン / CREB |
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| Research Abstract |
We reported that the expression of Ca2+ binding proteins, calbindin-D28k (CB) and parvalbumin correlates with the expression of Ca2+ permeable AMPA receptors (AMPA-Rs) in rat forebrain. We analyzed cell surface expression of a Ca2+ impermeable subunit, GluR2 and a Ca2+ permeable subunit, GluR2Q using an adenoviral-mediated expression system in COS7 cells. Biochemical measurements of cell surface expressed subunits using biotinylation experiments revealed that cell surface expression of GluR2Q is significantly increased with CB coexpression. By application of AMPA-R blockers, cell surface expression of GluR2Q is increased in the absence of CB coexpression. To determine whether Ca2+ entry via Ca2+ permeable AMPA receptor causes the suppression, we used the Ca2+ chelater, BAPTA-AM. Application of BAPTA-AM increases cell surface expression of GluR2Q. These results suggest that CB enhances cell surface expression of Ca2+ permeable AMPA-Rs by buffering the increased intracellular Ca2+ that enters through Ca2+ permeable AMPA-Rs.
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