| Project/Area Number |
16K09455
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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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| Research Field |
Cardiovascular medicine
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| Research Institution | Showa University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 交感神経 / 抑制作用 / 交感神経節前ニューロン / 脊髄中間外側核 / ノルアドレナリン / オートレセプター / 脊髄-交感神経幹摘出標本 / 交感神経システム / 循環器・高血圧 |
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| Outline of Final Research Achievements |
It was reported that NE depolarized the SPNs and NE significantly increased the frequency and voltage of EPSP and IPSP. Dxm after application of NE decreased the EPSP frequency and EPSP voltage and IPSP voltage of the SPN. However, in some SPNs, NE induced membrane hyperpolarization and completely inhibited firings. Dxm had no effect in these SPNs. Next, we tried similar experiments using medulla - spinal cord - sympathetic nerve trunk preparation to see clearly inhibitory effects via α2-adrenergic receptor. However, we could not have clear effects. Other agents (Phenylephrine、Atipamezole、Corticotrophin releasing factor) also did not show any clear effects. Based on the above, we are studying the mechanisms of regulation of glutamic acid release via α2 receptor by adrenergic C1 neuron.
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| Academic Significance and Societal Importance of the Research Achievements |
交感神経システムにおけるα2受容体を介した抑制作用についてはよくわかっていない。我々は、興奮下でオートレセプターによる抑制作用が機能しない場合、交感神経活動過亢進からカテコラミン過剰状態になり、心血管疾患の増悪に関与している可能性がある との仮説を立てた。本研究は交感神経の抑制作用を薬理学的、電気性生理学的に考察し、交感神経過亢進が引き起こす疾患においてもそのメカニズムの考察に重要と考えられる。
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