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Fluorescent Nanoparticles for the Measurement of Ion Concentration in Biological Systems
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Sodium sensing in the brain.

Masaharu Noda1, Takeshi Y Hiyama

  • 1Division of Molecular Neurobiology, National Institute for Basic Biology, 5-1 Higashiyama, Myodaiji-cho, Okazaki, 444-8787, Japan, madon@nibb.ac.jp.

Pflugers Archiv : European Journal of Physiology
|December 11, 2014
PubMed
Summary

The Nax channel in the brain acts as a sodium ([Na+]) sensor, regulating salt intake. Its activation involves glial cells and influences neuronal activity, with dysfunction linked to hypernatremia.

Area of Science:

  • Neuroscience
  • Physiology
  • Molecular Biology

Background:

  • Sodium (Na) homeostasis is vital, with body fluid Na+ levels tightly regulated between 135-145 mM.
  • The existence and molecular identity of a brain Na+ sensor remained elusive until the identification of the Nax channel.

Purpose of the Study:

  • To review the Na+ sensing mechanism in the brain for salt intake regulation.
  • To summarize research on the Nax channel's role in sensing physiological Na+ levels.

Main Methods:

  • Investigated Nax channel expression in circumventricular organs (CVOs), particularly the subfornical organ (SFO).
  • Examined the interaction of Nax with Na+/K+-ATPase and its effect on cellular metabolism.
  • Studied the role of endothelin-3 in modulating Nax sensitivity.

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  • Analyzed a case of hypernatremia linked to Nax autoimmunity.

    • Main Results:

    • Nax channels are expressed in astrocytes and ependymal cells in the SFO, a key site for salt intake control.
    • Nax activation is modulated by endothelin-3, enabling sensing within the physiological Na+ range.
    • Nax interacts with Na+/K+-ATPase, leading to ATP consumption and activation of anaerobic glucose metabolism in glial cells.
    • Lactate released from glial cells acts as a gliotransmitter, activating GABAergic neurons that influence salt intake behavior.
    • Autoimmunity against Nax can cause essential hypernatremia due to complement-mediated cell death in CVOs.

    Conclusions:

    • Nax is the molecular entity of the brain's Na+ sensor, crucial for regulating salt intake.
    • The Nax-mediated pathway involves glial cell metabolism and neurotransmission, linking Na+ sensing to behavioral output.
    • Nax dysfunction, as seen in autoimmunity, can lead to severe electrolyte imbalances like hypernatremia.