| Budget Amount *help |
¥232,440,000 (Direct Cost: ¥178,800,000、Indirect Cost: ¥53,640,000)
Fiscal Year 2017: ¥35,490,000 (Direct Cost: ¥27,300,000、Indirect Cost: ¥8,190,000)
Fiscal Year 2016: ¥35,490,000 (Direct Cost: ¥27,300,000、Indirect Cost: ¥8,190,000)
Fiscal Year 2015: ¥39,000,000 (Direct Cost: ¥30,000,000、Indirect Cost: ¥9,000,000)
Fiscal Year 2014: ¥63,570,000 (Direct Cost: ¥48,900,000、Indirect Cost: ¥14,670,000)
Fiscal Year 2013: ¥58,890,000 (Direct Cost: ¥45,300,000、Indirect Cost: ¥13,590,000)
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| Outline of Final Research Achievements |
We studied the pathophysiological mechanisms of increases in the intracellular Ca2+ concentration (Ca2+ signals) in the brain at levels between cell and whole body using new imaging methods, and obtained the following results. (1) Nitric oxide induces neuronal Ca2+ signals, which are involved in neuronal cell death following status epilepticus. We showed that the ryanodine receptor, which is the molecular basis of the nitric oxide-induced Ca2+ signals, can be a therapeutic target to protect neurons from cell death. (2) Upon neuronal injury, astrocytes generate Ca2+ signals releasing Ca2+ from the endoplasmic reticulum and promote neuroprotection. (3) We generated new indicators to visualize Ca2+ concentrations within the endoplasmic reticulum and mitochondria, and established the method to analyze the basis of generation of pathophysiological Ca2+ signals.
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