Neuronal mechanisms of the propofol-induced alpha rhythm
| Project/Area Number |
18K09731
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 57060:Surgical dentistry-related
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小林 真之 日本大学, 歯学部, 教授 (00300830)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | プロポフォール誘発性アルファ周波数帯 / 視床―皮質路 / 島皮質 / 視床後内側腹側核小細胞部 / 視床後内側腹側核小細胞部（VPMpc） / propofol / alpha-rhythm / insular cortex / VPMpc / thalamocortical input / プロポフォール |
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| Outline of Final Research Achievements |
Propofol enhanced unitary inhibitory postsynaptic currents recorded from the connection between fast-spiking (FS) neurons and pyramidal neurons in the rat insular cortex (IC). The synchronization index, which reflects the degree of spike synchronization among pyramidal neurons, was increased by propofol when a presynaptic FS neuron was activated at 10 Hz. AAV5.CAG.ChR2(H134R).mCherry, a virus that expresses ChR2 and a fluorescent protein in a anterograde manner, was injected into the medial parvicellular portion of the ventral posterior medial division of the thalamus (VPMpc), and their terminals were densely observed in layer 2/3 of the IC. Laser stimulation of ChR2-expressing thalamocortical terminals evoked excitatory postsynaptic currents (EPSCs) in both FS and pyramidal neurons. The latency, time to peak, and half width of EPSCs recorded from FS neurons were shorter than those recorded from pyramidal neurons.
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| Academic Significance and Societal Importance of the Research Achievements |
プロポフォールによる意識消失時にアルファ周波数帯（8～13 Hz）の増強が観察されることが分かっている一方で，その発生メカニズムの詳細は不明であった。本研究結果により，プロポフォールはFS細胞から錐体細胞への抑制性入力を増強することで錐体細胞の発火タイミングをアルファ周波数帯に近づける可能性が示唆された。また島皮質FS細胞はVPMpcからの興奮性入力を錐体細胞に先行して受けることで，周囲の錐体細胞を視床からの興奮性入力の前に抑制することで，発火タイミングの調節を行っている可能性が示唆された。これらの基礎的データの蓄積は，精度の高い麻酔・鎮静深度モニタの開発に寄与する可能性が考えられる。
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Report
(4 results)
Research Products
(3 results)
