Roles of 5-HT1A receptor in the expression of AMPA receptor and BDNF in developing mouse cortical neurons

The possible interactions between serotonergic and glutamatergic systems during neural development and under the pathogenesis of depression remain unclear. We now investigated roles of 5-HT1A receptor in the mRNA expression of AMPA receptor subunits (GluR1 and GluR2) and brain-derived neurotrophic factor (BDNF) using primary culture of cerebral cortex of mouse embryos. Neurons at embryonic day 18 were cultured for 3 days or 14 days and then treated with 5-HT1A receptor agonist (8-OH-DPAT) for 3 h or 24 h. In neurons cultured for 3 days, 8-OH-DPAT treatment for both 3 h and 24 h increased the mRNA levels of BDNF and GluR1, but not GluR2. In neurons cultured for 14 days, however, 8-OH-DPAT had no effects on these mRNA levels. Next, we examined in vivo roles of 5-HT1A receptor by administration of 8-OH-DPAT to newborn mice. Twenty-four hours after the oral administration of 8-OH-DPAT, the mRNA expression of BDNF was decreased in the frontal cortex, but had no effects on the mRNA expression of GluR1 and GluR2. Taken together, the present study suggests that 5-HT1A receptor activation modulates mRNA expression of AMPA receptor subunit and BDNF in cortical neurons, and the effects are different between in vitro and in vivo

Crystal Structures of a Piscine Betanodavirus: Mechanisms of Capsid Assembly and Viral Infection

Betanodaviruses cause massive mortality in marine fish species with viral nervous necrosis. The structure of a T = 3 Grouper nervous necrosis virus-like particle (GNNV-LP) is determined by the ab initio method with non-crystallographic symmetry averaging at 3.6 Å resolution. Each capsid protein (CP) shows three major domains: (i) the N-terminal arm, an inter-subunit extension at the inner surface; (ii) the shell domain (S-domain), a jelly-roll structure; and (iii) the protrusion domain (P-domain) formed by three-fold trimeric protrusions. In addition, we have determined structures of the T = 1 subviral particles (SVPs) of (i) the delta-P-domain mutant (residues 35−217) at 3.1 Å resolution; and (ii) the N-ARM deletion mutant (residues 35−338) at 7 Å resolution; and (iii) the structure of the individual P-domain (residues 214−338) at 1.2 Å resolution. The P-domain reveals a novel DxD motif asymmetrically coordinating two Ca2+ ions, and seems to play a prominent role in the calcium-mediated trimerization of the GNNV CPs during the initial capsid assembly process. The flexible N-ARM (N-terminal arginine-rich motif) appears to serve as a molecular switch for T = 1 or T = 3 assembly. Finally, we find that polyethylene glycol, which is incorporated into the P-domain during the crystallization process, enhances GNNV infection. The present structural studies together with the biological assays enhance our understanding of the role of the P-domain of GNNV in the capsid assembly and viral infection by this betanodavirus

2-5サイジ 二 オケル チョウカク ユウハツ ジバ ト ゲンゴ ノウリョク

This is the author's version of a work that was accepted for publication in European Journal of Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms, may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in European Journal of Neuroscience, VOLUME 35, ISSUE 4, 2012-02-09, DOI: 10.1111/j.1460-9568.2012.07998.

The relationship between Bloom and Stephen : a study of James Joyce's Ulysses

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Jonathan Wild, "Greater" than a Picaro

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Studies of Language Evolution for Co-creative Human Communication

金沢大学人間社会研究域学校教育系先行研究から、幼児期から学齢期の子どもにおいて、人の声「ね」によって引き起こされた脳反応が言語の概念的推論能力と関連することが報告されている。しかしながら、脳機能を計測する刺激として「ね」という音声のみを用いていたため、この関係が音声に特異的かどうかについては明らかになっていなかった。そこで、本研究では、純音刺激を用いて、5歳から7歳の63人の定型発達児を対象に、脳反応（P1m）と言語発達の関連を調べた。その結果、純音刺激によって引き起こされた脳反応は、振幅の大きさ、反応の潜時とも、左右半球ともに言語能力の指標とは有意な関係が認められなかった。本研究の結果から、幼児期から学齢期の子どもの言語発達において、「人の声」に対する脳内処理機構が深くかかわっていることが示唆された。対象児は、5歳から7歳の定型発達児（女児37人、男児26人）である。言語能力の指標として、K-ABCの下位検査である「表現ごい」「数唱」「なぞなぞ」を用いた。脳機能計測には、幼児用脳磁図（MEG）を用いた。聴覚刺激は、2種類の純音刺激を含む、オドボールパラダイムを用いた。脳機能の解析には、双極子推定法を用い、刺激提示後約100ms後に出現し、ダイポールの向きが前上方向である成分をP1mとして左右半球の聴覚野からそれぞれ抽出した。左右のP1mの振幅と反応がピークになる速さについて、言語能力との関連を調べた。ピアソンの相関解析では、右半球のP1mの振幅と言語の概念的推論能力（なぞなぞ）に有意な相関が認められた。しかしながら、月齢と言語の概念的推論能力（なぞなぞ）を独立変数に入れた重回帰分析の結果、その関係は有意には達しなかった。右半球のP1mの振幅と他の言語指標、潜時と言語指標、左半球のP1mの振幅および潜時と言語指標の間には、有意な関係は認められなかった。研究課題/領域番号:18H05067, 研究期間(年度):2018-04-01 – 2020-03-31出典：研究課題「自閉スペクトラム症幼児におけるコミュニケーション態度を伝達する音声処理の脳内基盤」課題番号18H05067,（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PUBLICLY-18H05067/）を加工して作

Developmental Trajectory of Infant Brain Signal Variability: A Longitudinal Pilot Study

The infant brain shows rapid neural network development that considerably influences cognitive and behavioral abilities in later life. Reportedly, this neural development process can be indexed by estimating neural signal complexity. However, the precise developmental trajectory of brain signal complexity during infancy remains elusive. This study was conducted to ascertain the trajectory of magnetoencephalography (MEG) signal complexity from 2 months to 3 years of age in five infants using multiscale entropy (MSE), which captures signal complexity at multiple temporal scales. Analyses revealed scale-dependent developmental trajectories. Specifically, signal complexity predominantly increased from 5 to 15 months of age at higher temporal scales, whereas the complexity at lower temporal scales was constant across age, except in one infant who showed decreased complexity. Despite a small sample size limiting this study’s power, this is the first report of a longitudinal investigation of changes in brain signal complexity during early infancy and is unique in its application of MSE analysis of longitudinal MEG data during infancy. The results of this pilot study may serve to further our understanding of the longitudinal changes in the neural dynamics of the developing infant brain

Joseph Andrews ノ ニジュウ コウゾウ : ミッツ ノ ソウワ ノ イギ

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