@phdthesis{oai:nagasaki-u.repo.nii.ac.jp:00003879,
 author = {馬場, 史郎},
 month = {Mar},
 note = {BDNF-TrkB signaling is implicated in experimental seizures and epilepsy. However, the downstream signaling involved in the epileptiform activity caused by TrkB receptor activation is still unknown. The aim of the present study was to determine whether TrkB-mediated N-Shc signal transduction was involved in kainic acid (KA)-induced epileptiform activity. We investigated KA-induced behavioral seizures, epileptiform activities and neuronal cell loss in hippocampus between N-Shc deficient and control mice. There was a significant reduction in seizure severity and the frequency of epileptiform discharges in N-Shc deficient mice, as compared with wild-type and C57BL/6 mice. KA-induced neuronal cell loss in the CA3 of hippocampus was also inhibited in N-Shc deficient mice. This study demonstrates that the activation of N-Shc signaling pathway contributes to an acute KA-induced epileptiform activity and neuronal cell loss in the hippocampus. We propose that the N-Shc-mediated signaling pathway could provide a potential target for the novel therapeutic approaches of epilepsy., 長崎大学学位論文 学位記番号:博(医歯薬)甲第933号 学位授与年月日:平成29年3月8日, Author: Shiro Baba, Kazuko Onga, Sho Kakizawa, Kyoji Ohyama, Kunihiko Yasuda, Hiroshi Otsubo, Brian W. Scott, W. McIntyre Burnham, Takayuki Matsuo, Izumi Nagata & Nozomu Mori, Citation: Scientific Reports, 6, 27511; 2016, Nagasaki University (長崎大学), 博士(医学) (2017-03-08)},
 school = {Nagasaki University (長崎大学)},
 title = {Involvement of the neuronal phosphotyrosine signal adaptor N-Shc in kainic acid-induced epileptiform activity},
 year = {2017}
}