• 作者：Yoshinori Mikami^a ; ^b ; Kazunori Kanemaru^a ; Yohei Okubo^a ; Takuya Nakaune^a ; Junji Suzuki^a ; Kazuki Shibata^c ; Hiroki Sugiyama^c ; Ryuta Koyama^c ; Takashi Murayama^d ; Akihiro Ito^e ; ^f ; Toshiko Yamazawa^g ; Yuji Ikegaya^c ; Takashi Sakurai^d ; Nobuhito Saito^e ; Sho Kakizawa^h ; ^{kakizawa.sho.4u@kyoto-u.ac.jp" class="auth_mail" title="E-mail the corresponding author} ; Masamitsu Iino^a ; ⁱ ; ^{iino@m.u-tokyo.ac.jp" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Ryanodine receptor ; Nitric oxide ; Calcium ; Seizures ; Neurodegeneration
• 刊名：EBioMedicine
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：11
• 期：Complete
• 页码：253-261
• 全文大小：1120 K

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NO-induced activation of RyR1 is critical for seizure-induced neuronal cell death.

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Dantrolene is protective against neurodegeneration caused by epileptic seizures.

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RyR1 is a therapeutic candidate to ameliorate the brain damage following seizures.

Status epilepticus (SE) is a life-threatening condition that can cause neurodegeneration. Mikami et al. report that NO-induced activation of type 1 ryanodine receptors (RyR1) is involved in SE-induced neuron death. Furthermore, dantrolene, an inhibitor of RyR1, has been found to be protective against neurodegeneration caused by SE.