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

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。目前关于低张力诱导的抑制机制的观点包括以下两种假设：渗透性肿胀的AVP神经元中拉伸失活阳离子通道（SIC）失活导致去极化减少，以及渗透性肿胀的胶质细胞释放牛磺酸后AVP神经元中甘氨酸受体（GlyR）激活导致超极化增加。在本研究中，大鼠AVP神经元未观察到SIC活性，在低渗条件下，牛磺酸诱导的GlyR激活只带来去极化而不带来超极化。此外，本研究表明，由细胞肿胀激活的牛磺酸释放阴离子通道可作为低渗的传感器。

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.