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KAKEN_17K15562seika.pdf
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Download
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:257.7 KB
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:Oct 31, 2019 |
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Total downloads since Oct 31, 2019 : 346
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神経伝達の新しい制御機構：活動依存的な細胞外イオン濃度の変化による制御機構の解明
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シンケイ デンタツ ノ アタラシイ セイギョ キコウ : カツドウ イゾンテキナ サイボウガイ イオン ノウド ノ ヘンカ ニ ヨル セイギョ キコウ ノ カイメイ
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Shinkei dentatsu no atarashii seigyo kikō : katsudō izontekina saibōgai ion nōdo no henka ni yoru seigyo kikō no kaimei
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The effect of extracellular Calcium dynamics on synaptic transmission
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荒井, 格
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アライ, イタル
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Arai, Itaru
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慶應義塾大学・医学部 (信濃町)・助教
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Research team head
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科研費研究者番号 : 00754631
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2019
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科学研究費補助金研究成果報告書
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2018
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小脳平行線維シナプスに発現するδ2型グルタミン酸受容体 (GluD2) はDセリンと結合することで同シナプス伝達を長期にわたって抑制する機能を持つ (DセリンLTD) が、Dセリン結合領域にCa2+ 結合部位を持つ。本研究では神経活動依存的なCa2+濃度変化がDセリンLTDに及ぼす影響を検討した。DセリンLTDは、誘発刺激を与える際の細胞外Ca2+濃度に依存して抑制された。一方、Ca2+結合能を阻害した変異型GluD2を持つノックインマウスではDセリンLTDは常に亢進していた。これらの結果から、GluD2の機能は神経活動に依存したCa2+濃度変化による制御を受けていることが示唆された。
Delta2 glutamate receptors (GluD2), which express in cerebellar parallel fiber - Purkinje cell synapses and induce long term depression by binding with D-serine (D-LTD), have Ca2+ binding sites at their ligand binding domain. In this study, I investigated how D-LTD is influenced by the extracellular Ca2+ concentration([Ca]o) dynamics during synaptic activities. When [Ca]o was reduced during the LTD induction, D-LTD was facilitated. On the other hand, D-LTD was inhibited when [Ca]o was elevated during its induction. Moreover, D-LTD was always facilitated when the similar experiments were performed by using knock in mice that have mutant GluD2 whose Ca2+ binding ability was disrupted. These results indicate that D-serine - GluD2 signaling is regulated by the [Ca]o dynamics during synaptic activities.
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研究種目 : 若手研究(B)
研究期間 : 2017～2018
課題番号 : 17K15562
研究分野 : 神経生理学
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