|
Affiliation |
Faculty of Medicine School of Medicine Department of Medical Sciences, Integrative Physiology |
|
Title |
Assistant Professor |
|
External Link |
|
UCHIDA Taku
|
|
|
Papers 【 display / non-display 】
-
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 2021.3
Language：English Publishing type：Research paper (scientific journal)
-
Abnormal γ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy Reviewed
Uchida T., Lossin C., Ihara Y., Deshimaru M., Yanagawa Y., Koyama S., Hirose S.
Epilepsia 58 ( 8 ) 1430 - 1439 2017.8
Language：English Publishing type：Research paper (scientific journal) Publisher：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
-
Ihara Y., Tomonoh Y., Deshimaru M., Zhang B., Uchida T., Ishii A., Hirose S.
PLoS ONE 11 ( 2 ) e0150095 2016.2
Language：English Publishing type：Research paper (scientific journal) Publisher：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.
-
Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse Reviewed
Uchida T, Furukawa T, Iwata S, Yanagawa Y, Fukuda A
Translational Psychiatry 2014.3
Language：English Publishing type：Research paper (scientific journal)
-
Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse Reviewed
Uchida T, Furukawa T, Iwata S, Yanagawa Y, Fukuda A
Translational Psychiatry 2014.3
Language：English Publishing type：Research paper (scientific journal)
Presentations 【 display / non-display 】
-
Effects of GluA1 gene mutation on AMPA receptor function found in Autism Spectrum Disorders with severe intellectual disability
NEURO2019
Event date： 2019.7.25 - 2019.7.28
Language：English Presentation type：Poster presentation
-
Increment of GABA neurotransmission in Kcnq2 gene mutation model of neonatal epilepsy International conference
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.
Event date： 2019.5.31 - 2019.6.1
Language：English Presentation type：Oral presentation (general)
Venue：Nagoya Congress Center, Japan
-
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）
Event date： 2017.7.20 - 2017.7.23
Language：Japanese Presentation type：Poster presentation
Venue：幕張メッセ 〒261-8550 千葉市美浜区中瀬2-1
-
Abnormal GABA neurotransmission in a Kcnq2 model of early-onset epilepsy International conference
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）
-
Abnormal GABA neurotransmission in a Kcnq2 model of early-onset epilepsy International conference
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
Event date： 2017.5.11 - 2017.5.14
Language：English Presentation type：Poster presentation
Venue：Hilton Fukuoka Sea Hawk FUKUOKA-SHI, 2-2-3 JIGYOHAMA, CHUO-KU, JAPAN
Grant-in-Aid for Scientific Research 【 display / non-display 】
-
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
Grant number：21K07757 2021.04 - 2025.03
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)
Authorship：Principal investigator
-
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
Grant number：21K07483 2021.04 - 2024.03
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、
Authorship：Coinvestigator(s)
-
KCNQ2遺伝子変異に起因する小児てんかんの病態解明
2014.04 - 2018.03
科学研究費補助金 若手研究(B)
Authorship：Principal investigator