Component

NMDA-type glutamate receptors

NMDA receptor ion-channel family; early native-neuron studies did not specify modern subunit combinations.

6 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 it acts on

  1. Blocking NMDA receptors, calcium influx or calpain abolished SSC and glutamate toxicity in primary murine neurons.

    NMDA-type glutamate receptors → Neuronal excitotoxic cell death source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"}
    experimental_model
    Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice
    exposure
    SSC/sulfite exposure; receptor/calcium/calpain inhibition
    limitations
    Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus neurons and mice; chemical reaction assays
    plain_language
    Interrupting several points in the chain prevented damage in this model.
    primary_references
    [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    tissue_or_cell_type
    Neuronal receptors, intracellular calcium and inhibitory synapses
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1327–1338

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice · source_derived_draft · unverified_draft

    ### mo-ssc-blockade Blocking NMDA receptors, calcium influx or calpain abolished SSC and glutamate toxicity in primary murine neurons. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Interrupting several points in the chain prevented damage in this model. organism: Mus musculus neurons and mice; chemical reaction assays tissue_or_cell_type: Neuronal receptors, intracellular calcium and inhibitory synapses experimental_model: Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice limitations: Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity. exposure: SSC/sulfite exposure; receptor/calcium/calpain inhibition evidence_span: {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"} [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    Complete structured claim and evidence

What acts on it

  1. SSC acted as an NMDA-receptor agonist in primary murine neurons.

    S-Sulfocysteine → NMDA-type glutamate receptors source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"}
    experimental_model
    Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice
    exposure
    SSC/sulfite exposure; receptor/calcium/calpain inhibition
    limitations
    Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus neurons and mice; chemical reaction assays
    plain_language
    A sulfur metabolite can imitate an excitatory neurotransmitter.
    primary_references
    [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    tissue_or_cell_type
    Neuronal receptors, intracellular calcium and inhibitory synapses
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1249–1260

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice · source_derived_draft · unverified_draft

    ### mo-ssc-nmda SSC acted as an NMDA-receptor agonist in primary murine neurons. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sulfur metabolite can imitate an excitatory neurotransmitter. organism: Mus musculus neurons and mice; chemical reaction assays tissue_or_cell_type: Neuronal receptors, intracellular calcium and inhibitory synapses experimental_model: Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice limitations: Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity. exposure: SSC/sulfite exposure; receptor/calcium/calpain inhibition evidence_span: {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"} [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    Complete structured claim and evidence

Where it participates (unsigned role)

  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. Combined NMDA- and AMPA-receptor blockade almost completely suppressed SSC-evoked currents, supporting SSC agonism at both receptor classes.

    S-Sulfocysteine → AMPA-type glutamate receptors source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/29106383.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7cfb311498ba2a88e3fc04be988dcffda740bbd1d93ada686cabf801861cf2a", "start_char": 16686, "end_char": 17024, "text_sha256": "bc275c8c18044e88885db4ff2c7ebbca4376b6e4c1b7b88b66385a33c7775b5b"}
    experimental_model
    Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice
    exposure
    SSC/sulfite exposure; receptor/calcium/calpain inhibition
    limitations
    Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus neurons and mice; chemical reaction assays
    plain_language
    More than one excitatory receptor contributed to the electrical response.
    primary_references
    [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    tissue_or_cell_type
    Neuronal receptors, intracellular calcium and inhibitory synapses
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1262–1273

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice · source_derived_draft · unverified_draft

    ### mo-ssc-ampa Combined NMDA- and AMPA-receptor blockade almost completely suppressed SSC-evoked currents, supporting SSC agonism at both receptor classes. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: More than one excitatory receptor contributed to the electrical response. organism: Mus musculus neurons and mice; chemical reaction assays tissue_or_cell_type: Neuronal receptors, intracellular calcium and inhibitory synapses experimental_model: Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice limitations: Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity. exposure: SSC/sulfite exposure; receptor/calcium/calpain inhibition evidence_span: {"source_cache": "artifacts/molybdenum-research/29106383.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7cfb311498ba2a88e3fc04be988dcffda740bbd1d93ada686cabf801861cf2a", "start_char": 16686, "end_char": 17024, "text_sha256": "bc275c8c18044e88885db4ff2c7ebbca4376b6e4c1b7b88b66385a33c7775b5b"} [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    Complete structured claim and evidence

  4. SSC receptor activation caused neuronal calcium influx.

    S-Sulfocysteine → Neuronal calcium influx source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"}
    experimental_model
    Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice
    exposure
    SSC/sulfite exposure; receptor/calcium/calpain inhibition
    limitations
    Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus neurons and mice; chemical reaction assays
    plain_language
    Receptor activation opens the way for calcium to enter.
    primary_references
    [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    tissue_or_cell_type
    Neuronal receptors, intracellular calcium and inhibitory synapses
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1275–1286

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice · source_derived_draft · unverified_draft

    ### mo-ssc-calcium SSC receptor activation caused neuronal calcium influx. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Receptor activation opens the way for calcium to enter. organism: Mus musculus neurons and mice; chemical reaction assays tissue_or_cell_type: Neuronal receptors, intracellular calcium and inhibitory synapses experimental_model: Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice limitations: Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity. exposure: SSC/sulfite exposure; receptor/calcium/calpain inhibition evidence_span: {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"} [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    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