Elucidation of hypotonicity-induced suppression mechanism of vasopressin secretion through identification of hypoosmolarity sensor

通过鉴定低渗透压传感器阐明低渗引起的加压素分泌抑制机制

• 批准号: 23659118
• 负责人: OKADA Yasunobu
• 金额: $ 2.41万
• 依托单位: National Institute for Physiological Sciences
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23659118/
• 关键词: 浸透圧センサー; バソプレシン視索上核; アニオンチャネル; タウリン; グリシンレセプター; 低浸透圧センサー; バソプレシン; 視索上核

Arginine-vasopressin (AVP), an antidiuretic hormone, is secreted from AVP neurons in a manner sensitive to body fluid osmolarity. The current view for the hypotonicity-induced suppression mechanism consists of following two hypotheses: Reduced depolarization due to inactivation of stretch-inactivated cation channel (SIC) in osmotically swollen AVP neurons, and increased hyperpolarization due to glycine receptor (GlyR) activation in AVP neurons in response to taurine released from osmotically swollen glial cells. In rat AVP neurons, in the present study, the SIC activity was not observed, and taurine-induced activation of GlyR brought about depolarization but not hyperpolarization under hypotonic conditions. Also, the present study showed that taurine-releasing anion channel activated by cell swelling serves as a sensor for hypoosmolarity.

精氨酸加压素（AVP）是一种抗利尿激素，由AVP神经元以对体液渗透压敏感的方式分泌。目前对低渗引起的抑制机制的观点包括以下两种假设：由于牵张性肿胀的AVP神经元中的牵张失活阳离子通道（SIC）失活而导致的去极化减少，以及由于AVP神经元中的甘氨酸受体（GlyR）响应于从牵张性肿胀的胶质细胞释放的牛磺酸而激活而导致的超极化增加。在大鼠AVP神经元中，在本研究中，SIC活动没有观察到，牛磺酸诱导的GlyR激活引起去极化，但不超极化低渗条件下。此外，本研究表明，牛磺酸释放阴离子通道激活细胞肿胀作为传感器的低渗透压。

项目成果

Volume-regulatory autocrine action of vasopressin released from somata and dendrites in vasopressin neurons is mediated by the V2 receptor and cAMP

加压素神经元体细胞和树突释放的加压素的容量调节自分泌作用由 V2 受体和 cAMP 介导

• 发表时间: 2011
• 作者: Kaori Sato;Tomohiro Numata;Takeshi Saito;Yoichi Ueta;Yasunobu Okada
• 通讯作者: Yasunobu Okada

Involvements of the ABC protein ABCF2 and α-actinin-4 in regulation of cell volume and anion channels in human epithelial cells

• DOI: 10.1002/jcp.24050
• 发表时间: 2012-10-01
• 期刊: JOURNAL OF CELLULAR PHYSIOLOGY
• 影响因子: 5.6
• 作者: Ando-Akatsuka, Yuhko;Shimizu, Takahiro;Okada, Yasunobu
• 通讯作者: Okada, Yasunobu

生理学研究所HP&機能協関研究部門 HP:公開日 2013.01.31 抗酸化物質グルタチオンが細胞から放出 される「通り道」を発見:Sabirov RZ, Kurbannazarova RS, Melanova NR, Okada Y. Volume-sensitive anion channels mediate osmosensitive glutathione release from rat thymocytes. PLoS One, 2013

国立生理科学研究所 HP 和功能协作研究部 HP：出版日期 2013.01.31 发现细胞释放抗氧化剂谷胱甘肽的“途径”：Sabirov RZ、Kurbannazarova RS、Melanova NR、Okada Y. 体积敏感阴离子通道介导大鼠胸腺细胞的渗透敏感性谷胱甘肽释放 PLoS One，2013 年。

Study on the hypoosmolarity sensing mechanism in arginine-vasopressin neurons: Reexamination on the taurine hypothesis

精氨酸-加压素神经元低渗感知机制的研究：牛磺酸假说的重新审视

• 发表时间: 2013
• 作者: Kaori Sato-Numata;Yoichi Ueta and Yasunobu Okada
• 通讯作者: Yoichi Ueta and Yasunobu Okada

sensing mechanism in arginine-vasopressin neurons : Reexamination on the taurine hypothesis

精氨酸-加压素神经元的传感机制：重新审视牛磺酸假说

• 发表时间: 2013
• 作者: K. Sato-Numata;Y. Ueta;Y. Okada
• 通讯作者: Y. Okada