| Project/Area Number |
25861283
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
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| Research Institution | Nagasaki University |
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Principal Investigator |
BABA Shiro 長崎大学, 病院(医学系), 客員研究員 (30530430)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | NShc / epilepsy / TrkB receptor / BDNF / kainic acid / hippocampus / neuronal cell death / seizure / N-Shc / TrkB |
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| Outline of Final Research Achievements |
BDNF-TrkB signaling is implicated in experimental seizures and epilepsy. However, the downstream signaling mechanism in epileptiform activity and epileptogenesis caused by TrkB activation is still controversial. Signaling at the TrkB-Shc site is transmitted through the neural-specific phosphotyrosine signal adaptor NShc. Therefore, the aim of this study is to examine whether NShc-mediated signaling pathway is involved in kainic acid (KA)-induced epileptiform activity.
We show a significant reduction of both seizure severity and frequency of epileptiform discharges in NShc deficient mice as compared with control mice. KA-induced neuronal cell loss in the CA3 area of hippocampus was also inhibited in NShc deficient mice. These results suggest that NShc is involved in KA-induced epileptiform activity. We propose that the NShc-mediated signaling pathway could provide a potential target for the development of novel therapeutic drugs and/or approaches in the treatment of epilepsy.
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