| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Because we could not find the evidence that shootin1 is involved in the aberrant axonal branch formation of hippocampal granule cells after epileptic seizure, we investigated the function of activity-dependent proteins in seizure-mediated axonal branching. We found that overexpression of neuritin, one of the protein increased after the seizures, promoted axonal branching in granule cells. Chemical kindling induced less severe seizures in neuritin knockout mice than in wild-type mice, and neuritin knockout mice showed smaller number of axonal branching after the induction of epileptic seizures.
We found that excess amount of Neuritin recruited FGF receptors to cell surface and the recruitment of FGF receptors activated FGF signaling. Furthermore, the increased activity of FGF signaling promoted axonal branching in granule cells.
We concluded that Neuritin-mediated translocation of FGF receptors induce abberant axonal branching after epileptic seizures.
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