Component
Rat NMDA-type glutamate receptors, subunits unresolved
Rat NMDA-type glutamate receptors, subunits unresolved. Species, exposure and limitations are retained in each linked claim.
7 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 acts on it
Extracellular agmatine blocked NMDA currents in rat hippocampal neurons in a voltage- and concentration-dependent manner; estimated pore-site Kd was 952 micromolar at 0 mV.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Cultured rat hippocampal neurons; whole-cell patch clamp.
- limitations
- The inferred pore site is not a solved binding structure or measured oral human brain exposure.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- Its glutamate-receptor effect depends on electrical conditions and concentration.
- primary_references
- Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 260–266
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cultured rat hippocampal neurons; whole-cell patch clamp. · source_derived_draft · unverified_draft
## agmatine-sulfate-nmda-block Its glutamate-receptor effect depends on electrical conditions and concentration. Extracellular agmatine blocked NMDA currents in rat hippocampal neurons in a voltage- and concentration-dependent manner; estimated pore-site Kd was 952 micromolar at 0 mV. Model: Cultured rat hippocampal neurons; whole-cell patch clamp. Limitations: The inferred pore site is not a solved binding structure or measured oral human brain exposure. Evidence access: Primary abstract Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Complete structured claim and evidencePutrescine had little NMDA-blocking effect compared with agmatine or arcaine in the same experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat neuron comparison of guanidine-containing and diamine compounds.
- limitations
- The result supports structural specificity; it does not measure metabolic conversion during recording.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- Converting agmatine to a related amine can change channel activity.
- primary_references
- Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 276–282
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat neuron comparison of guanidine-containing and diamine compounds. · source_derived_draft · unverified_draft
## agmatine-sulfate-putrescine-nmda Converting agmatine to a related amine can change channel activity. Putrescine had little NMDA-blocking effect compared with agmatine or arcaine in the same experiments. Model: Rat neuron comparison of guanidine-containing and diamine compounds. Limitations: The result supports structural specificity; it does not measure metabolic conversion during recording. Evidence access: Primary abstract Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Complete structured claim and evidenceSpermine still potentiated NMDA current in the presence of agmatine, supporting distinct interaction sites for the two compounds.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat hippocampal-neuron electrophysiology.
- limitations
- This is a cellular interaction, not evidence that co-supplementation is beneficial.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- Two connected polyamine-related molecules can push the same channel in different directions.
- primary_references
- Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 268–274
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat hippocampal-neuron electrophysiology. · source_derived_draft · unverified_draft
## agmatine-sulfate-spermine-nmda Two connected polyamine-related molecules can push the same channel in different directions. Spermine still potentiated NMDA current in the presence of agmatine, supporting distinct interaction sites for the two compounds. Model: Rat hippocampal-neuron electrophysiology. Limitations: This is a cellular interaction, not evidence that co-supplementation is beneficial. Evidence access: Primary abstract Agmatine selectively blocks the N-methyl-D-aspartate subclass of glutamate receptor channels in rat hippocampal neurons. · 1999 · https://pubmed.ncbi.nlm.nih.gov/9918557/
Complete structured claim and evidenceKynurenic-acid NMDA-blocking IC50 shifted from about 15 to 235 micromolar when 10 micromolar glycine was present.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat neuronal electrophysiological assay.
- limitations
- An assay co-agonist effect does not show that glycine supplements change human disease outcomes.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A second amino acid changed how strongly the metabolite blocked a receptor.
- primary_references
- The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 314–320
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat neuronal electrophysiological assay. · source_derived_draft · unverified_draft
## tryptophan-glycine-kyna-nmda A second amino acid changed how strongly the metabolite blocked a receptor. Kynurenic-acid NMDA-blocking IC50 shifted from about 15 to 235 micromolar when 10 micromolar glycine was present. Model: Rat neuronal electrophysiological assay. Limitations: An assay co-agonist effect does not show that glycine supplements change human disease outcomes. Evidence access: Primary abstract The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
Complete structured claim and evidenceAdding 30 micromolar magnesium reduced quinolinate-activated NMDA channel mean open time to about one-third at minus 100 mV.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat hippocampal patch-clamp experiment.
- limitations
- Does not establish that oral magnesium prevents quinolinate-related disease.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Magnesium and membrane voltage changed the receptor response.
- primary_references
- Quinolinate activation of N-methyl-D-aspartate ion channels in rat hippocampal neurons. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1700844/ · DOI 10.1016/0304-3940(90)90098-t
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 282–288
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat hippocampal patch-clamp experiment. · source_derived_draft · unverified_draft
## tryptophan-magnesium-nmda Magnesium and membrane voltage changed the receptor response. Adding 30 micromolar magnesium reduced quinolinate-activated NMDA channel mean open time to about one-third at minus 100 mV. Model: Rat hippocampal patch-clamp experiment. Limitations: Does not establish that oral magnesium prevents quinolinate-related disease. Evidence access: Primary abstract Quinolinate activation of N-methyl-D-aspartate ion channels in rat hippocampal neurons. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1700844/ · DOI 10.1016/0304-3940(90)90098-t
Complete structured claim and evidenceQuinolinate at 75 micromolar opened NMDA channels in cultured rat hippocampal neurons in calcium-containing, magnesium-free recording solution.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat CA1 neuronal single-channel recording; 1.8 mM calcium.
- limitations
- Quinolinate is not tryptophan itself; bath concentration is not a dietary dose.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- One downstream metabolite activates an excitatory receptor.
- primary_references
- Quinolinate activation of N-methyl-D-aspartate ion channels in rat hippocampal neurons. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1700844/ · DOI 10.1016/0304-3940(90)90098-t
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 274–280
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat CA1 neuronal single-channel recording; 1.8 mM calcium. · source_derived_draft · unverified_draft
## tryptophan-quinolinate-nmda One downstream metabolite activates an excitatory receptor. Quinolinate at 75 micromolar opened NMDA channels in cultured rat hippocampal neurons in calcium-containing, magnesium-free recording solution. Model: Rat CA1 neuronal single-channel recording; 1.8 mM calcium. Limitations: Quinolinate is not tryptophan itself; bath concentration is not a dietary dose. Evidence access: Primary abstract Quinolinate activation of N-methyl-D-aspartate ion channels in rat hippocampal neurons. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1700844/ · DOI 10.1016/0304-3940(90)90098-t
Complete structured claim and evidenceTheanine inhibited radioligand binding at NMDA glycine-site sites in rat cortical preparations.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/12596867.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaa387f7967a1ff8e68eceb71fd3294881967066c5dc080fd27bacf8a01ce33d", "start_char": 0, "end_char": 643, "text_sha256": "eaa387f7967a1ff8e68eceb71fd3294881967066c5dc080fd27bacf8a01ce33d"}
- experimental_model
- Radioligand receptor-binding competition
- exposure
- Theanine competition with radiolabeled ligands
- limitations
- Binding displacement is not proof of functional agonism/antagonism at an oral human dose. Abstract wording for the 80-30000-fold IC50 comparison is ambiguous and is not used as a potency estimate.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Rat cortical preparations
- plain_language
- A binding assay identifies a possible receptor interaction while leaving functional and clinical effects unresolved.
- primary_references
- [theanine-p12596867] Inhibition by theanine of binding of [3H]AMPA, [3H]kainate, and [3H]MDL 105,519 to glutamate receptors. (2002). https://pubmed.ncbi.nlm.nih.gov/12596867/ DOI: 10.1271/bbb.66.2683
- tissue_or_cell_type
- AMPA, kainate and NMDA glycine-site binding
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 315–326
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioligand receptor-binding competition · source_derived_draft · unverified_draft
### theanine-binding-nmda Theanine inhibited radioligand binding at NMDA glycine-site sites in rat cortical preparations. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A binding assay identifies a possible receptor interaction while leaving functional and clinical effects unresolved. organism: Rat cortical preparations tissue_or_cell_type: AMPA, kainate and NMDA glycine-site binding experimental_model: Radioligand receptor-binding competition limitations: Binding displacement is not proof of functional agonism/antagonism at an oral human dose. Abstract wording for the 80-30000-fold IC50 comparison is ambiguous and is not used as a potency estimate. exposure: Theanine competition with radiolabeled ligands evidence_span: {"source_cache": "artifacts/theanine-research/12596867.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaa387f7967a1ff8e68eceb71fd3294881967066c5dc080fd27bacf8a01ce33d", "start_char": 0, "end_char": 643, "text_sha256": "eaa387f7967a1ff8e68eceb71fd3294881967066c5dc080fd27bacf8a01ce33d"} [theanine-p12596867] Inhibition by theanine of binding of [3H]AMPA, [3H]kainate, and [3H]MDL 105,519 to glutamate receptors. (2002). https://pubmed.ncbi.nlm.nih.gov/12596867/ DOI: 10.1271/bbb.66.2683
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.