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医学部 医学科 機能制御学講座統合生理学分野 |
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Fhod3 Controls the Dendritic Spine Morphology of Specific Subpopulations of Pyramidal Neurons in the Mouse Cerebral Cortex.
Sulistomo HW, Nemoto T, Kage Y, Fujii H, Uchida T, Takamiya K, Sumimoto H, Kataoka H, Bito H, Takeya R
Cerebral cortex (New York, N.Y. : 1991) 31 ( 4 ) 2205 - 2219 2021年3月
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Abnormal γ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy 査読あり
Uchida T., Lossin C., Ihara Y., Deshimaru M., Yanagawa Y., Koyama S., Hirose S.
Epilepsia 58 ( 8 ) 1430 - 1439 2017年8月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Epilepsia
Wiley Periodicals, Inc. © 2017 International League Against Epilepsy Objective: Mutations of the KCNQ2 gene, which encodes the Kv7.2 subunit of voltage-gated M-type potassium channels, have been associated with epilepsy in the neonatal period. This developmental stage is unique in that the neurotransmitter gamma aminobutyric acid (GABA), which is inhibitory in adults, triggers excitatory action due to a reversed chloride gradient. Methods: To examine whether KCNQ2-related neuronal hyperexcitability involves neonatally excitatory GABA, we examined 1-week-old knockin mice expressing the Kv7.2 variant p.Tyr284Cys (Y284C). Results: Brain slice electrophysiology revealed elevated CA1 hippocampal GABAergic interneuron activity with respect to presynaptic firing and postsynaptic current frequency. Blockade with the GABAAreceptor antagonist bicuculline decreased ictal-like bursting in brain slices with lowered divalent ion concentration, which is consistent with GABA mediating an excitatory function that contributes to the hyperexcitability observed in mutant animals. Significance: We conclude that excitatory GABA contributes to the phenotype in these animals, which raises the question of whether this special type of neurotransmission has broader importance in neonatal epilepsy than is currently recognized.
DOI： 10.1111/epi.13807
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Ihara Y., Tomonoh Y., Deshimaru M., Zhang B., Uchida T., Ishii A., Hirose S.
PLoS ONE 11 ( 2 ) e0150095 2016年2月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：PLoS ONE
© 2016 Ihara et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The hetero-tetrameric voltage-gated potassium channel Kv7.2/Kv7.3, which is encoded by KCNQ2 and KCNQ3, plays an important role in limiting network excitability in the neonatal brain. Kv7.2/Kv7.3 dysfunction resulting from KCNQ2 mutations predominantly causes self-limited or benign epilepsy in neonates, but also causes early onset epileptic encephalopathy. Retigabine (RTG), a Kv7.2/Kv7.3-channel opener, seems to be a rational antiepileptic drug for epilepsies caused by KCNQ2 mutations. We therefore evaluated the effects of RTG on seizures in two strains of knock-in mice harboring different Kcnq2 mutations, in comparison to the effects of phenobarbital (PB), which is the first-line antiepileptic drug for seizures in neonates. The subjects were heterozygous knock-in mice (Kcnq2Y284C/+and Kcnq2A306T/+) bearing the Y284C or A306T Kcnq2 mutation, respectively, and their wildtype (WT) littermates, at 63-100 days of age. Seizures induced by intraperitoneal injection of kainic acid (KA, 12mg/kg) were recorded using a video-electroencephalography (EEG) monitoring system. Effects of RTG on KA-induced seizures of both strains of knock-in mice were assessed using seizure scores from a modified Racine's scale and compared with those of PB. The number and total duration of spike bursts on EEG and behaviors monitored by video recording were also used to evaluate the effects of RTG and PB. Both Kcnq2Y284C/+and Kcnq2A306T/+mice showed significantly more KA-induced seizures than WT mice. RTG significantly attenuated KA-induced seizure activities in both Kcnq2Y284C/+and Kcnq2A306T/+mice, and more markedly than PB. This is the first reported evidence of RTG ameliorating KA-induced seizures in knock-in mice bearing mutations of Kcnq2,with more marked effects than those observed with PB. RTG or other Kv7.2-channel openers may be considered as first-line antiepileptic treatments for epilepsies resulting from KCNQ2 mutations.
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Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse 査読あり
Uchida T, Furukawa T, Iwata S, Yanagawa Y, Fukuda A
Translational Psychiatry 2014年3月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse 査読あり
Uchida T, Furukawa T, Iwata S, Yanagawa Y, Fukuda A
Translational Psychiatry 2014年3月
記述言語：英語 掲載種別：研究論文（学術雑誌）
講演・口頭発表等 【 表示 ／ 非表示 】
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知的障害を伴う自閉症スペクトラム障害に見られるGluA1遺伝子変異がAMPA受容体に与える影響
Taku Uchida, Ryosuke Midorikawa, Kogo Takamiya
第42回日本神経科学大会
開催年月日： 2019年7月25日 - 2019年7月28日
記述言語：英語 会議種別：ポスター発表
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Increment of GABA neurotransmission in Kcnq2 gene mutation model of neonatal epilepsy 国際会議
Taku Uchida, Christoph Lossin, Yukiko Ihara, Masanobu Deshimaru, Yuchio Yanagawa, Susumu Koyama, Shinichi Hirose
20th Annual Meeting of Infantile Seizure Society (ISS) (Nagoya Congress Center, Japan) Akihisa Okumura, M.D.
開催年月日： 2019年5月31日 - 2019年6月1日
記述言語：英語 会議種別：口頭発表（一般）
開催地：Nagoya Congress Center, Japan
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Abnormal GABA neurotransmission in a Kcnq2 model of early-onset epilepsy
Taku Uchida, Masanobu Deshimaru, Yuchio Yanagawa, Susumu Koyama, Shinichi Hirose
第40回日本神経科学学会 (幕張メッセ 〒261-8550 千葉市美浜区中瀬2-1) 狩野 方伸（東京大学大学院医学系研究科）
開催年月日： 2017年7月20日 - 2017年7月23日
記述言語：日本語 会議種別：ポスター発表
開催地：幕張メッセ 〒261-8550 千葉市美浜区中瀬2-1
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Abnormal GABA neurotransmission in a Kcnq2 model of early-onset epilepsy 国際会議
Taku Uchida, Masanobu Deshimaru, Yuchio Yanagawa, Susumu Koyama, Shinichi Hirose
第40回日本神経科学学会 (幕張メッセ 〒261-8550 千葉市美浜区中瀬2-1) 狩野 方伸（東京大学大学院医学系研究科）
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Abnormal GABA neurotransmission in a Kcnq2 model of early-onset epilepsy 国際会議
Taku Uchida, Christoph Lossin, Yukiko Ihara, Masanobu Deshimaru, Yuchio Yanagawa, Susumu Koyama, Shinichi Hirose
14th Asian and Oceanian Congress of Child Neurology (Hilton Fukuoka Sea Hawk FUKUOKA-SHI, 2-2-3 JIGYOHAMA, CHUO-KU, JAPAN) Department of Pediatrics, Fukuoka University
開催年月日： 2017年5月11日 - 2017年5月14日
記述言語：英語 会議種別：ポスター発表
開催地：Hilton Fukuoka Sea Hawk FUKUOKA-SHI, 2-2-3 JIGYOHAMA, CHUO-KU, JAPAN
科研費（文科省・学振・厚労省）獲得実績 【 表示 ／ 非表示 】
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GRIA1遺伝子変異が関与する自閉スペクトラム症の病態解明
研究課題/領域番号：21K07757 2021年04月 - 2025年03月
独立行政法人日本学術振興会 科学研究費補助金 基盤研究(C)
担当区分：研究代表者
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グルタミン酸受容体の糖鎖修飾による脳高次機能と精神疾患への関与
研究課題/領域番号：21K07483 2021年04月 - 2024年03月
独立行政法人日本学術振興会 科学研究費補助金 基盤研究(C)
高宮 考悟、
担当区分：研究分担者
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KCNQ2遺伝子変異に起因する小児てんかんの病態解明
2014年04月 - 2018年03月
科学研究費補助金 若手研究(B)
担当区分：研究代表者
寄附金・講座・研究部門 【 表示 ／ 非表示 】
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統合生理学分野研究奨学金(公益財団法人川野小児医学奨学財団令和２年度（第31回）研究助成)
寄附者名称：公益財団法人川野小児医学奨学財団 2020年07月