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This Article Full Text Full Text (PDF) All Versions of this Article: 92/3/513    most recent expphysiol.2006.035659v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Noda, M. Search for Related Content PubMed PubMed Citation Articles by Noda, M. Related Collections Symposia Papers

¹ Division of Molecular Neurobiology, National Institute for Basic Biology and School of Life Science, Graduate University for Advanced Studies, Okazaki 444-8787, Japan

Abstract

Dehydration causes an increase in the sodium (Na) concentration and osmolarity of body fluids. For Na homeostasis of the body, control of Na and water intake and excretion are of prime importance. Although the circumventricular organs (CVOs) were suggested to be involved in body-fluid homeostasis, the system for sensing Na levels within the brain, which is responsible for the control of Na- and water-intake behaviour, has long been an enigma. Na_x is an atypical sodium channel that is assumed to be a descendant of the voltage-gated sodium channel family. Our studies on the Na_x-gene-targeting (Na_x^–/–) mouse revealed that Na_x channels are localized to the CVOs and serve as a sodium-level sensor of body fluids. As the first step to understand the cellular mechanism by which the information sensed by Na_x channels is reflected in the activity of the organs, we dissected the subcellular distribution of Na_x. Double-immunostaining and immuno-electron microscopic analyses revealed that Na_x is exclusively localized to perineuronal lamellate processes extending from ependymal cells and astrocytes in the organs. In addition, glial cells isolated from the subfornical organ were sensitive to an increase in the extracellular sodium level, as analysed by an ion-imaging method. These results suggest that glial cells bearing Na_x channels are the first to sense a physiological increase in the level of sodium in body fluids, and regulate the neural activity of the CVOs by enveloping neurons. Close communication between inexcitable glial cells and excitable neural cells thus appears to be the basis of the central control of salt homeostasis.

(Received 11 January 2007; accepted after revision 28 February 2007; first published online 9 March 2007)
Corresponding author M. Noda: Division of Molecular Neurobiology, National Institute for Basic Biology, 5-1 Higashiyama, Myodaiji-cho, Okazaki 444-8787, Japan. Email: madon{at}nibb.ac.jp

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