Role of clutch protein shootin1 in activity-dependent axonal elongation

2015 Fiscal Year Final Research Report

• Project/Area Number: 24700349
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neuroscience in general
• Research Institution: Tokyo Metropolitan Institute of Medical Science
• Principal Investigator: SHIMADA Tadayuki 公益財団法人東京都医学総合研究所, 脳発達・神経再生分野, 主席研究員 (80379552)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: てんかん / 軸索分枝 / 神経回路 / ＦＧＦシグナル

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.

Free Research Field

神経科学