Component

NMDA receptor-mediated current

Agonist-evoked cation current through NMDA receptor channels.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Removing extracellular Mg reduced voltage dependence and relieved inward NMDA current block in cultured mouse spinal neurons.

    Mg2+ → NMDA receptor-mediated current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence-system
    Voltage clamp; extracellular Mg withdrawal
    experimental_model
    Voltage clamp; extracellular Mg withdrawal
    exposure
    Withdrawal of approximately 1 mM extracellular Mg from neuronal bathing fluid; not a dietary or serum exposure.
    limitations
    Experimental bath depletion is distinct from low intake, serum hypomagnesemia or measured brain Mg depletion.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Loss of extracellular magnesium removes a brake on excitatory current in this preparation.
    primary_references
    [mayer-1984-nmda] Voltage-dependent block by Mg2+ of NMDA responses in spinal cord neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6325946/ DOI: 10.1038/309261a0
    tissue
    Cultured spinal cord neurons
    tissue_or_cell_type
    Cultured spinal cord neurons
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1274–1286

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Voltage clamp; extracellular Mg withdrawal · source_derived_draft · unverified_draft

    ### low-bath-magnesium-relieves-nmda-block Removing extracellular Mg reduced voltage dependence and relieved inward NMDA current block in cultured mouse spinal neurons. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of extracellular magnesium removes a brake on excitatory current in this preparation. organism: Mouse tissue_or_cell_type: Cultured spinal cord neurons experimental_model: Voltage clamp; extracellular Mg withdrawal limitations: Experimental bath depletion is distinct from low intake, serum hypomagnesemia or measured brain Mg depletion. exposure: Withdrawal of approximately 1 mM extracellular Mg from neuronal bathing fluid; not a dietary or serum exposure. evidence-system: Voltage clamp; extracellular Mg withdrawal tissue: Cultured spinal cord neurons [mayer-1984-nmda] Voltage-dependent block by Mg2+ of NMDA responses in spinal cord neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6325946/ DOI: 10.1038/309261a0
    Complete structured claim and evidence

  2. Extracellular Mg caused voltage-dependent block of NMDA-type currents in cultured mouse neurons, stronger at hyperpolarized potentials.

    Mg2+ → NMDA receptor-mediated current source_derived_draftungraded
    Experimental context and source evidence
    evidence-system
    Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes
    experimental_model
    Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes
    limitations
    Native channel subunits were not resolved; no nutritional intake or clinical outcome was tested.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Magnesium restrains this excitatory current in a way that depends on membrane voltage.
    primary_references
    [nowak-1984-nmda] Magnesium gates glutamate-activated channels in mouse central neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6320006/ DOI: 10.1038/307462a0
    tissue
    Cultured central neurons
    tissue_or_cell_type
    Cultured central neurons

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1261–1272

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes · source_derived_draft · unverified_draft

    ### magnesium-voltage-dependent-nmda-block Extracellular Mg caused voltage-dependent block of NMDA-type currents in cultured mouse neurons, stronger at hyperpolarized potentials. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium restrains this excitatory current in a way that depends on membrane voltage. organism: Mouse tissue_or_cell_type: Cultured central neurons experimental_model: Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes limitations: Native channel subunits were not resolved; no nutritional intake or clinical outcome was tested. evidence-system: Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes tissue: Cultured central neurons [nowak-1984-nmda] Magnesium gates glutamate-activated channels in mouse central neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6320006/ DOI: 10.1038/307462a0
    Complete structured claim and evidence

  3. Fyn kinase is a determinant of ethanol sensitivity through its relation to NMDA receptor function, with tyrosine phosphorylation of the receptor linked to acute tolerance.

    Tyrosine-protein kinase Fyn → NMDA receptor-mediated current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/9381182.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "008253b9262aee0b3acd845dfea4f9c087c00e0078bd1ba9b4eaa265192ec782", "start_char": 0, "end_char": 742, "text_sha256": "008253b9262aee0b3acd845dfea4f9c087c00e0078bd1ba9b4eaa265192ec782"}
    experimental_model
    Fyn-null mice with NMDA receptor phosphorylation measurement
    exposure
    Ethanol sensitivity and tyrosine phosphorylation in Fyn-deficient mice
    limitations
    Links acute tolerance to a specific kinase. The behavioural readout is hypnotic sensitivity, not drinking.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Mouse
    plain_language
    A kinase decides how quickly the receptor adapts, and so how quickly tolerance appears.
    primary_references
    [alcohol-p9381182] Fyn-kinase as a determinant of ethanol sensitivity: relation to NMDA-receptor function. (1997). https://pubmed.ncbi.nlm.nih.gov/9381182/ DOI: 10.1126/science.278.5338.698
    tissue_or_cell_type
    Hippocampus
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 306–317

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fyn-null mice with NMDA receptor phosphorylation measurement · source_derived_draft · unverified_draft

    ### alcohol-fyn-tolerance Fyn kinase is a determinant of ethanol sensitivity through its relation to NMDA receptor function, with tyrosine phosphorylation of the receptor linked to acute tolerance. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: A kinase decides how quickly the receptor adapts, and so how quickly tolerance appears. organism: Mouse tissue_or_cell_type: Hippocampus experimental_model: Fyn-null mice with NMDA receptor phosphorylation measurement limitations: Links acute tolerance to a specific kinase. The behavioural readout is hypnotic sensitivity, not drinking. exposure: Ethanol sensitivity and tyrosine phosphorylation in Fyn-deficient mice evidence_span: {"source_cache": "artifacts/alcohol-research/9381182.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "008253b9262aee0b3acd845dfea4f9c087c00e0078bd1ba9b4eaa265192ec782", "start_char": 0, "end_char": 742, "text_sha256": "008253b9262aee0b3acd845dfea4f9c087c00e0078bd1ba9b4eaa265192ec782"} [alcohol-p9381182] Fyn-kinase as a determinant of ethanol sensitivity: relation to NMDA-receptor function. (1997). https://pubmed.ncbi.nlm.nih.gov/9381182/ DOI: 10.1126/science.278.5338.698
    Complete structured claim and evidence

  4. Ethanol inhibited NMDA-activated ion current in hippocampal neurons at concentrations reached during intoxication.

    Ethanol → NMDA receptor-mediated current source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/2467382.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c968c9a63cb2826e3986e1fd13f83fdf231adc1d46e0bc9aa73882cce6f0dca1", "start_char": 0, "end_char": 844, "text_sha256": "c968c9a63cb2826e3986e1fd13f83fdf231adc1d46e0bc9aa73882cce6f0dca1"}
    experimental_model
    Whole-cell recording from dissociated hippocampal neurons
    exposure
    Ethanol at intoxicating concentrations applied to NMDA-activated current
    limitations
    The founding electrophysiology result for this target. Concentrations are in the intoxicating range, which is what makes it relevant to drinking.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Rat
    plain_language
    Alcohol shuts down the brain’s main excitatory receptor at the doses people actually drink.
    primary_references
    [alcohol-p2467382] Ethanol inhibits NMDA-activated ion current in hippocampal neurons. (1989). https://pubmed.ncbi.nlm.nih.gov/2467382/ DOI: 10.1126/science.2467382
    tissue_or_cell_type
    Hippocampal neurons

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 280–291

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-cell recording from dissociated hippocampal neurons · source_derived_draft · unverified_draft

    ### alcohol-nmda-inhibition Ethanol inhibited NMDA-activated ion current in hippocampal neurons at concentrations reached during intoxication. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Alcohol shuts down the brain’s main excitatory receptor at the doses people actually drink. organism: Rat tissue_or_cell_type: Hippocampal neurons experimental_model: Whole-cell recording from dissociated hippocampal neurons limitations: The founding electrophysiology result for this target. Concentrations are in the intoxicating range, which is what makes it relevant to drinking. exposure: Ethanol at intoxicating concentrations applied to NMDA-activated current evidence_span: {"source_cache": "artifacts/alcohol-research/2467382.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c968c9a63cb2826e3986e1fd13f83fdf231adc1d46e0bc9aa73882cce6f0dca1", "start_char": 0, "end_char": 844, "text_sha256": "c968c9a63cb2826e3986e1fd13f83fdf231adc1d46e0bc9aa73882cce6f0dca1"} [alcohol-p2467382] Ethanol inhibits NMDA-activated ion current in hippocampal neurons. (1989). https://pubmed.ncbi.nlm.nih.gov/2467382/ DOI: 10.1126/science.2467382
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards