Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 25 January 2011
Vol. 4, Issue 157, p. ra5
[DOI: 10.1126/scisignal.2001279]


V2 Receptor–Mediated Autocrine Role of Somatodendritic Release of AVP in Rat Vasopressin Neurons Under Hypo-Osmotic Conditions

Kaori Sato1,2, Tomohiro Numata2*, Takeshi Saito3, Yoichi Ueta3, and Yasunobu Okada1,2{dagger}

1 Department of Physiological Sciences, School of Life Science, Graduate University for Advanced Studies (SOKENDAI), Okazaki 444-8585, Japan.
2 Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
3 Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.

* Present address: Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University, Katsura Campus, Kyoto 615-8510, Japan.

Abstract: 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 V2-type vasopressin receptor. The V2 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 V2 receptor was present in AVP neurons. We conclude that somatodendritic release of AVP under hypo-osmotic conditions acts through the V2 receptor as an autocrine signal to enhance volume-sensitive anion channel activity and thereby facilitate cell volume regulation.

{dagger} To whom correspondence should be addressed. E-mail: okada{at}

Citation: K. Sato, T. Numata, T. Saito, Y. Ueta, Y. Okada, V2 Receptor–Mediated Autocrine Role of Somatodendritic Release of AVP in Rat Vasopressin Neurons Under Hypo-Osmotic Conditions. Sci. Signal. 4, ra5 (2011).

Read the Full Text

DCPIB, the Proposed Selective Blocker of Volume-Regulated Anion Channels, Inhibits Several Glutamate Transport Pathways in Glial Cells.
N. H. Bowens, P. Dohare, Y.-H. Kuo, and A. A. Mongin (2013)
Mol. Pharmacol. 83, 22-32
   Abstract »    Full Text »    PDF »
Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems.
T.-a. Koshimizu, K. Nakamura, N. Egashira, M. Hiroyama, H. Nonoguchi, and A. Tanoue (2012)
Physiol Rev 92, 1813-1864
   Abstract »    Full Text »    PDF »
Epithelial Na+ sodium channels in magnocellular cells of the rat supraoptic and paraventricular nuclei.
R. Teruyama, M. Sakuraba, L. L. Wilson, N. E. J. Wandrey, and W. E. Armstrong (2012)
Am J Physiol Endocrinol Metab 302, E273-E285
   Abstract »    Full Text »    PDF »
Science Signaling Podcast: 25 January 2011.
S. Wakino, Y. Okada, and A. M. VanHook (2011)
Science Signaling 4, pc2
   Abstract »    Full Text »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882