Component

Extracellular brain glutamate concentration

Extracellular brain glutamate concentration

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.

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. Acute symptomatic rats had thalamic dialysate glutamate of 3.37 versus 0.93 micromolar in controls, with no corresponding cortical increase.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Abstract
    evidence_span
    precedes the appearance of histological lesions
    experimental_model
    Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls.
    exposure
    Pyrithiamine-induced deficiency within six hours of loss of righting reflexes
    limitations
    Microdialysis alone cannot assign increased release versus impaired uptake or prove NMDA-mediated cell death. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Glutamate accumulated outside cells in a vulnerable region before visible tissue lesions.
    primary_references
    [hazell-1993-extracellular-glutamate] Cerebral vulnerability is associated with selective increase in extracellular glutamate concentration in experimental thiamine deficiency (1993). https://pubmed.ncbi.nlm.nih.gov/8103080/ DOI: 10.1111/j.1471-4159.1993.tb03635.x
    tissue_or_cell_type
    Ventral posterior medial thalamus versus frontoparietal cortex
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1141–1153

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls. · source_derived_draft · unverified_draft

    ### thiamine-def-thalamic-extracellular-glutamate Acute symptomatic rats had thalamic dialysate glutamate of 3.37 versus 0.93 micromolar in controls, with no corresponding cortical increase. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutamate accumulated outside cells in a vulnerable region before visible tissue lesions. organism: Rattus norvegicus tissue_or_cell_type: Ventral posterior medial thalamus versus frontoparietal cortex experimental_model: Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls. limitations: Microdialysis alone cannot assign increased release versus impaired uptake or prove NMDA-mediated cell death. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold. evidence_location: Abstract evidence_span: precedes the appearance of histological lesions exposure: Pyrithiamine-induced deficiency within six hours of loss of righting reflexes [hazell-1993-extracellular-glutamate] Cerebral vulnerability is associated with selective increase in extracellular glutamate concentration in experimental thiamine deficiency (1993). https://pubmed.ncbi.nlm.nih.gov/8103080/ DOI: 10.1111/j.1471-4159.1993.tb03635.x
    Complete structured claim and evidence
  2. Sustained 10 mM theanine lowered extracellular glutamate released from cultured neurons.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/theanine-research/18293419.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c94471071feadec8a04eafa7e9d53999dd9756b7f1d5dc1f351152b9b5f4b5d3", "start_char": 0, "end_char": 1751, "text_sha256": "c94471071feadec8a04eafa7e9d53999dd9756b7f1d5dc1f351152b9b5f4b5d3"}
    experimental_model
    Radiotracer uptake in synaptosomes and cultured neural cells
    exposure
    Theanine 0.1-10 millimolar in uptake assays; sustained 10 millimolar for glutamate release
    limitations
    High cell concentrations; 10 mM is far above the approximately 25 micromolar plasma peak in the separate human 100 mg study. Different cells from the system L screen; no claim all routes are sodium-dependent.
    nutrient_topic
    L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
    organism
    Rat neurons and astroglia
    plain_language
    A high-concentration cell result is preserved without presenting it as a proven effect of an ordinary oral dose.
    primary_references
    [theanine-p18293419] Theanine, an ingredient of green tea, inhibits [3H]glutamine transport in neurons and astroglia in rat brain. (2008). https://pubmed.ncbi.nlm.nih.gov/18293419/ DOI: 10.1002/jnr.21637
    tissue_or_cell_type
    Glutamine transport and extracellular glutamate

    L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 263–274

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiotracer uptake in synaptosomes and cultured neural cells · source_derived_draft · unverified_draft

    ### theanine-glutamate-release Sustained 10 mM theanine lowered extracellular glutamate released from cultured neurons. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A high-concentration cell result is preserved without presenting it as a proven effect of an ordinary oral dose. organism: Rat neurons and astroglia tissue_or_cell_type: Glutamine transport and extracellular glutamate experimental_model: Radiotracer uptake in synaptosomes and cultured neural cells limitations: High cell concentrations; 10 mM is far above the approximately 25 micromolar plasma peak in the separate human 100 mg study. Different cells from the system L screen; no claim all routes are sodium-dependent. exposure: Theanine 0.1-10 millimolar in uptake assays; sustained 10 millimolar for glutamate release evidence_span: {"source_cache": "artifacts/theanine-research/18293419.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c94471071feadec8a04eafa7e9d53999dd9756b7f1d5dc1f351152b9b5f4b5d3", "start_char": 0, "end_char": 1751, "text_sha256": "c94471071feadec8a04eafa7e9d53999dd9756b7f1d5dc1f351152b9b5f4b5d3"} [theanine-p18293419] Theanine, an ingredient of green tea, inhibits [3H]glutamine transport in neurons and astroglia in rat brain. (2008). https://pubmed.ncbi.nlm.nih.gov/18293419/ DOI: 10.1002/jnr.21637
    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