Project/Area Number |
11308032
|
Research Category |
Grant-in-Aid for Scientific Research (A).
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | The University of Tokyo |
Principal Investigator |
MIKOSHIBA Katsuhiko The Institute of Medical Science Department of Basic Medical Sciences The University of Tokyo. Professor., 医科学研究所, 教授 (30051840)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥36,000,000 (Direct Cost: ¥36,000,000)
Fiscal Year 2000: ¥15,400,000 (Direct Cost: ¥15,400,000)
Fiscal Year 1999: ¥20,600,000 (Direct Cost: ¥20,600,000)
|
Keywords | IP_3 / Ca^<2+> / endoplasmic reticulum / レーザー光 / マラカイトグリーン / IP3 / IP_3受容体 / 神経成長円錐 / LTD / LTP / 神経可塑性 / レーザー / Ca^<2+> |
Research Abstract |
We have found that wave and Ca2+ oscillation is produced through the Ca2+ channel localized on the endoplasmic reticulum which is a Ca2+ store site inside the cell, and not through Ca2+ channel on the plasma membrane. We used CALI(chromophore assisted laser inactivation)method using laser beam to study if IP3 receptor mediated Ca2+ movement is involved in growth cone formation and neurite extention. We used malakite green to label specific antibody against type 1 IP3 receptor. We added laser beam to the dye to produce redicals. While control antibody showed no block in neurite extention, antibody against type IP3 showed retraction of neurite, only when laser is added at growth cone. This suggests that IP3 receptor medited Ca2+ release is involved in neurite extention.
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