The inhibitory mechanism of AVP release under hypoosmotic conditions
| Project/Area Number |
26860153
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Fukuoka University (2015-2017)
National Institute for Physiological Sciences (2014) |
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Principal Investigator |
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| Research Collaborator |
OKADA Yasunobu 京都府立医科大学, 医学部, 特任教授 (10025661)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ＡＶＰニューロン / 低浸透圧 / タウリン / アストロサイト / イオンチャネル / 細胞容積 / バソプレシン / アニオンチャネル / 阻害剤 / バソプレシンニューロン |
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| Outline of Final Research Achievements |
We checked substances secreted under hypotonic conditions using primary cultured astrocytes collected from the rat SON region, and found that glutamic acid and aspartic acid are secreted in addition to taurine. Exposure of taurine or GABA to vasopressin neurons under hypotonic conditions suppressed spontaneous excitation despite membrane depolarization. The effect on membrane potential and spontaneous excitation by taurine exposure was abolished with inhibitors of GABAA receptors or glycine receptors but was not affected by inhibitors of GABAB receptors. From these results suggest ed that the effect on taurine to membrane depolarization and suppression of spontaneous excitation is occurred via glycine receptor and GABAA receptors.
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Report
(5 results)
Research Products
(11 results)
