Gliotransmitter release and its protective effects in spinal astrocytes
Project/Area Number |
26450440
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Integrative animal science
|
Research Institution | Hokkaido University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
YAMAGUCHI Soichiro 北海道大学, 大学院獣医学研究科, 助教 (50596864)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | アストロサイト / アデノシン / 硫化水素 / 脊髄 / グリア伝達物質 / 低酸素 / シスタチオニンβシンターゼ / シスタチオンβシンターゼ / 平衡ヌクレオシド輸送体 / 平衡ヌクレオチド輸送体 / ギャップジャンクションヘミチャネル / アデノシンキナーゼ |
Outline of Final Research Achievements |
Production and release mechanisms of adenosine and hydrogen sulfide (H2S), which are known to be neuroprotective agents, were examined in the cultured spinal astrocytes. Under the low Ca2+ conditions, ATP released by astrocytes was extracellularly degraded to adenosine, resulting in the increase in extracellular adenosine level. The astrocytic CBS (H2S synthase) expression was suggested to be controlled/maintained by the neurons. Adenosine and H2S affect cellular functions via the activation of receptors and ion channels. Under the ischemic conditions, it is suggested that the change in adenosine and H2S production and releases by the low Ca2+ and/or neuronal death is involved in disease onset and progression.
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Report
(4 results)
Research Products
(31 results)