Component
Mouse sodium-sensing channel Nax / Scn7a
Mouse sodium-sensing channel Nax / Scn7a. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
The sodium-associated increase in SFO lactate production occurred in wild-type but not Nax-knockout mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"}
- experimental_model
- Protein interaction, glial metabolism and SFO neuronal recordings
- exposure
- Elevated sodium; Nax knockout; lactate exposure
- limitations
- Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Mouse SFO and mammalian cell preparations
- plain_language
- Glial cells turn a sodium signal into a metabolic signal carried by lactate.
- primary_references
- [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
- tissue_or_cell_type
- Glial cells and GABAergic neurons of the subfornical organ
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 460–471
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein interaction, glial metabolism and SFO neuronal recordings · source_derived_draft · unverified_draft
### sodium-nax-lactate The sodium-associated increase in SFO lactate production occurred in wild-type but not Nax-knockout mice. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glial cells turn a sodium signal into a metabolic signal carried by lactate. organism: Mouse SFO and mammalian cell preparations tissue_or_cell_type: Glial cells and GABAergic neurons of the subfornical organ experimental_model: Protein interaction, glial metabolism and SFO neuronal recordings limitations: Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold. exposure: Elevated sodium; Nax knockout; lactate exposure evidence_span: {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"} [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
Complete structured claim and evidenceNax directly interacted with sodium/potassium-pump alpha subunits in the study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"}
- experimental_model
- Protein interaction, glial metabolism and SFO neuronal recordings
- exposure
- Elevated sodium; Nax knockout; lactate exposure
- limitations
- Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Mouse SFO and mammalian cell preparations
- plain_language
- A sodium-sensing channel can connect sodium detection to the cell’s energy use.
- primary_references
- [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
- tissue_or_cell_type
- Glial cells and GABAergic neurons of the subfornical organ
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 447–458
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein interaction, glial metabolism and SFO neuronal recordings · source_derived_draft · unverified_draft
### sodium-nax-pump Nax directly interacted with sodium/potassium-pump alpha subunits in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-sensing channel can connect sodium detection to the cell’s energy use. organism: Mouse SFO and mammalian cell preparations tissue_or_cell_type: Glial cells and GABAergic neurons of the subfornical organ experimental_model: Protein interaction, glial metabolism and SFO neuronal recordings limitations: Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold. exposure: Elevated sodium; Nax knockout; lactate exposure evidence_span: {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"} [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.