The inhibitory mechanism of AVP release under hypoosmotic conditions

2017 Fiscal Year Final Research Report

• Project/Area Number: 26860153
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General physiology
• Research Institution: Fukuoka University (2015-2017); National Institute for Physiological Sciences (2014)
• Principal Investigator: Sato-Numata Kaori (佐藤かお理) 福岡大学, 医学部, 特別研究員(RPD) (60614196)
• Research Collaborator: OKADA Yasunobu 京都府立医科大学, 医学部, 特任教授 (10025661)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: ＡＶＰニューロン / 低浸透圧 / タウリン / アストロサイト

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.

Free Research Field

細胞生理学