ReviewPflugers Archiv : European journal of physiology2015
Sodium sensing in the brain.
Review in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Plasticity of subfornical organ astrocyte structure and supraoptic nucleus hormone expression following extreme dehydration in the desert rodent Gerbillus tarabuli.Journal of neuroendocrinology · 2026Article
- Dravet Syndrome Patient-Derived Neural Cells Present Altered Levels of Potassium, Copper, and Zinc.ACS chemical neuroscience · 2026Article
- Sex differences in central salt sensing in the human brain.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Mechanisms of intrinsic osmolality and sodium detection by magnocellular neurosecretory neurons.Journal of neuroendocrinology · 2025Review
- Central nervous system mechanisms of salt-sensitive hypertension.Physiological reviews · 2025Review
- Actin fenestrae amplify the membrane response to hypertonic stress in osmosensory neurons.iScience · 2025Article
- Recent advances in bio-integrated electrochemical sensors for neuroengineering.Fundamental research · 2025Review
- Autoimmunity related to anti-NaEndocrine journal · 2024Review
- Brain sodium sensing for regulation of thirst, salt appetite, and blood pressure.Physiological reports · 2024Review
- Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Anti-ZSCAN1 Autoantibodies Are a Feasible Diagnostic Marker for ROHHAD Syndrome Not Associated with a Tumor.International journal of molecular sciences · 2024Article
- NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The organum vasculosum of the lamina terminalis and subfornical organ: regulation of thirst.Frontiers in neuroscience · 2023Review
- Autoimmunity Related to Adipsic Hypernatremia and ROHHAD Syndrome.International journal of molecular sciences · 2022Review
- Hypernatremia in brain-dead patients.Brain and behavior · 2022Article
- Dietary sodium and health: How much is too much for those with orthostatic disorders?Autonomic neuroscience : basic & clinical · 2022Review
- Central regulation of body fluid homeostasis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022Review
- Glial functions in the blood-brain communication at the circumventricular organs.Frontiers in neuroscience · 2022Review
- Sodium MR Neuroimaging.AJNR. American journal of neuroradiology · 2021Review
- Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake.Nature communications · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium (Na) homeostasis is crucial for life, and the Na(+) level ([Na(+)]) of body fluids is strictly maintained at a range of 135-145 mM. However, the existence of a [Na(+)] sensor in the brain has long been controversial until Nax was identified as the molecular entity of the sensor. This review provides an overview of the [Na(+)]-sensing mechanism in the brain for the regulation of salt intake by summarizing a series of our studies on Nax. Nax is a Na channel expressed in the circumventricular organs (CVOs) in the brain. Among the CVOs, the subfornical organ (SFO) is the principal site for the control of salt intake behavior, where Nax populates the cellular processes of astrocytes and ependymal cells enveloping neurons. A local expression of endothelin-3 in the SFO modulates the [Na(+)] sensitivity for Nax activation, and thereby Nax is likely to be activated in the physiological [Na(+)] range. Nax stably interacts with Na(+)/K(+)-ATPase whereby Na(+) influx via Nax is coupled with activation of Na(+)/K(+)-ATPase associated with the consumption of ATP. The consequent activation of anaerobic glucose metabolism of Nax-positive glial cells upregulates the cellular release of lactate, and this lactate functions as a gliotransmitter to activate GABAergic neurons in the SFO. The GABAergic neurons presumably regulate hypothetic neurons involved in the control of salt intake behavior. Recently, a patient with essential hypernatremia caused by autoimmunity to Nax was found. In this case, the hypernatremia was considered to be induced by the complement-mediated cell death in the CVOs, where Nax specifically populates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.