| Project/Area Number |
20791084
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | University of Miyazaki |
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Principal Investigator |
YONAHA Tetsu University of Miyazaki, 医学部, 助教 (70468023)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 麻酔薬 / 睡眠経路 / 脳神経核 / パッチクランプ |
|---|
| Research Abstract |
Propofol and muscimol inhibited TMN neuron activity mediated by GABAA-receptor. Dexmedetomidine (DEX) inhibited TMN neuronal activity mediated by α_2-receptor. P, muscimol, and DEX induced high-amplitude and slow wave on the EEG, and immobilization on the EMG. Sevoflurane decreased firing frequency of TMN. DEX decreased the neuronal firing rate of LC neuron, however, little hyperpolarization and only a small reduction of the input resistance of the neurons were seen. Higher concentrations of dexmedetomidine resulted not only in a greater inhibition of firing but also in the hyperpolarization of the membrane and a decreased input resistance. The α_2-adrenergic receptor antagonist, yohimbine (100 nM), partially blocked the dexmedetomidine-induced hyperpolarization. The application of yohimbine produced a parallel, dose-related shift to the right of the dexmedetomidine dose-response curve. The hyperpolarizing effect of DEX was antagonized by tertiapin. DEX decreased membrane potential mediated by activation of G-protein coupled inwardly rectified K channels (GIRK). The hyperpolarizing effect of P on the VLPO was larger than in LC and TMN.
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