1996 Fiscal Year Final Research Report Summary
Role of IP3 receptor in CA2+ signaling and development and differentiation
| Project/Area Number |
07408021
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIKOSHIBA Katsuhiko The University of Tokyo, Inst, Medical Science, Professor, 医科学研究所, 教授 (30051840)
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| Project Period (FY) |
1995 – 1996
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| Keywords | IP3 / IP3 receptor / calcium / endoplasmic reticulum / epilepsy / cerebellar ataxia / gene targeting / cerebellum |
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| Research Abstract |
The inositol 1,4,5-trisphosphate (IP3) receptor acts as an IP3-gated Ca2+ release channel in a variety of cell types. Yupe 1 IP3 receptor (IP3R) is the major neuronal member of the IP3R family in the central nervous system, predominantly enriched in cerebellar Purkinje cells but also concentrated in neurons in the hippocampal CA1 region, caudate-putamen, and cerebral cortex. Here we report that most IP3R1- deficient mice geberated by gene targeting die in utero, and born animals have severe ataxia and tonic or tonic-clonic seizures and die by the wearing geriod. An electroncephalogram showed that they suffer from epilepsy, indicating that IP3R1 is essential for proper brain function. However, observation by light microscope of the haematoxylin-eosin staining of the brain and peripheral tissues of IP3R1-deficient mice showed no abnormality, and the unique electrophysiological properties of the cerebellar Purkinje cells of IP3R1-deficient mice were not severely impaired.
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