| Budget Amount *help |
¥215,800,000 (Direct Cost: ¥166,000,000、Indirect Cost: ¥49,800,000)
Fiscal Year 2017: ¥40,560,000 (Direct Cost: ¥31,200,000、Indirect Cost: ¥9,360,000)
Fiscal Year 2016: ¥40,560,000 (Direct Cost: ¥31,200,000、Indirect Cost: ¥9,360,000)
Fiscal Year 2015: ¥44,590,000 (Direct Cost: ¥34,300,000、Indirect Cost: ¥10,290,000)
Fiscal Year 2014: ¥44,200,000 (Direct Cost: ¥34,000,000、Indirect Cost: ¥10,200,000)
Fiscal Year 2013: ¥45,890,000 (Direct Cost: ¥35,300,000、Indirect Cost: ¥10,590,000)
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| Outline of Final Research Achievements |
IP3 receptor (IP3R)-deficient mice exhibit cerebellar ataxia, epileptic seizure-like symptom and retardation of neuronal development. However, it was a longstanding controversy if IP3R/Ca2+ signaling is involved in neuronal plasticity. We generated knock-out mice of all IP3R isoforms (IP3R1-3), and knock-out mice with region- or neuron-specific deletion of IP3R1. Mice lacking IP3R1 in Purkinje neurons demonstrated regulation of CaMKII/actin cytoskeleton/spine formation by IP3R1 (PNAS). LTP regulation by transport machines of IP3R1-coding mRNA (Nature Neurosci), modulatory roles of glial IP3R2 on gliotransmitter release to regulate neuronal functions (Nature Commun, J Clinical Invest), protein quality control by IP3R-associating ERp44 (Mol Cell) were also discovered. Much evidence, including GABA receptor regulation (Cell Rep) and apoptosis regulation by IP3R-bound IRBIT (eLIFE, PNAS), strongly indicates that IP3R controls synaptic plasticity.
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