Department of Physiological Sciences, School of Life Science, Graduate University for Advanced Studies (SOKENDAI), Okazaki 444-8585, Japan.
Sci Signal. 2011 Jan 25;4(157):ra5. doi: 10.1126/scisignal.2001279.
Arginine vasopressin (AVP) neurons in the hypothalamus are osmosensory neurons that respond to increased or decreased plasma osmolarity by releasing more or less AVP, respectively, from their axon terminals. Here, we found that, in contrast, hypo-osmotic stress enhanced somatodendritic AVP secretion from isolated rat AVP neurons, and this somatodendritic release depended on actin depolymerization. In AVP neurons identified by transgenic expression of green fluorescent protein, hypo-osmotic stimulation led to activation of anion currents and a slow regulatory volume decrease (RVD). Bath application of AVP increased the volume-sensitive anion current and accelerated RVD; these effects were abolished by inhibition of adenylate cyclase or by a specific antagonist of the V(2)-type vasopressin receptor. The V(2) receptor antagonist slowed the RVD rate of AVP neurons even in the absence of exogenous AVP when the volume of bath solution was reduced. Reverse transcription polymerase chain reaction and immunostaining both indicated that the V(2) receptor was present in AVP neurons. We conclude that somatodendritic release of AVP under hypo-osmotic conditions acts through the V(2) receptor as an autocrine signal to enhance volume-sensitive anion channel activity and thereby facilitate cell volume regulation.
下丘脑的精氨酸加压素（AVP）神经元是渗透压感受器神经元，它们通过从轴突末梢分别释放更多或更少的 AVP 来响应血浆渗透压的增加或减少。在这里，我们发现，与上述情况相反，低渗应激增强了从分离的大鼠 AVP 神经元中传出的体树突 AVP 分泌，并且这种体树突释放依赖于肌动蛋白解聚。在通过转绿色荧光蛋白（GFP）表达鉴定的 AVP 神经元中，低渗刺激导致阴离子电流激活和缓慢的调节性容积减少（RVD）。AVP 的浴液应用增加了体积敏感的阴离子电流并加速了 RVD；这些效应被抑制环腺苷酸酶或 V2 型加压素受体的特异性拮抗剂所消除。当浴液体积减少时，即使没有外源性 AVP，V2 受体拮抗剂也会减缓 AVP 神经元的 RVD 速率。逆转录聚合酶链反应和免疫染色均表明 V2 受体存在于 AVP 神经元中。我们的结论是，低渗条件下的 AVP 体树突释放通过 V2 受体作为自分泌信号发挥作用，增强体积敏感的阴离子通道活性，从而促进细胞容积调节。
