| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Laboratory of Neurophysiology, National Institute for Basic Biology, Okazaki, Aichi, Japan; School of Life Science, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan
2 Division of Molecular Neurobiology, National Institute for Basic Biology, Okazaki, Aichi, Japan; School of Life Science, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan
3 Laboratory of Morphodiversity, National Institute for Basic Biology, Okazaki, Aichi, Japan; School of Life Science, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan
4 Department of Applied Biology, Kyoto Institute for Technology, Sakyo, Kyoto, Japan
5 Department of Genetic and Behavioral Neuroscience, Gunma University, Maebashi, Gunma, Japan
6 RIKEN Brain Science Institute, Wako, Saitama, Japan
* To whom correspondence should be addressed. E-mail: madon{at}nibb.ac.jp.
Nax is an atypical sodium channel that is assumed to be a descendant of the voltage-gated sodium channel family. Our recent studies on the N
x-gene targeting mouse revealed that Nax channel is localized to the circumventricular organs (CVOs), the central loci for the salt and water homeostasis in mammals, where Nax channel serves as a sodium-level sensor of the body fluid. To understand the cellular mechanism by which the information sensed by Nax channels is transferred to the activity of the organs, we dissected the subcellular localization of Nax in the present study. Double-immunostaining and immunoelectron microscopic analyses revealed that Nax is exclusively localized to perineuronal lamellate processes extended from ependymal cells and astrocytes in the organs. In addition, glial cells isolated from the subfornical organ, one of the CVOs, were sensitive to an increase in the extracellular sodium level, as analyzed by an ion-imaging method. These results suggest that glial cells bearing Nax channel are the first to sense a physiological increase in the level of sodium in the body fluid, 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 the salt homeostasis.
This article has been cited by other articles:
|
|
 |
|
  J. C. Geerling and A. D. Loewy Central regulation of sodium appetite Exp Physiol, February 1, 2008; 93(2): 177 - 209. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. N. Orlov and A. A. Mongin Salt-sensing mechanisms in blood pressure regulation and hypertension Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2039 - H2053. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Noda Hydromineral Neuroendocrinology: Hydromineral neuroendocrinology: mechanism of sensing sodium levels in the mammalian brain Exp Physiol, May 1, 2007; 92(3): 513 - 522. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
