Component

The blood-brain barrier

The blood-brain barrier. Species, exposure and limitations are retained in each linked claim.

2 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

Where it participates (unsigned role)

  1. GABA transport was studied by cellular uptake of tritiated GABA which was sodium-, chloride- and concentration-dependent with a Michaelis-Menten constant of 679 plus or minus 80 micromol per litre and a maximal uptake rate of 4,790 pmol per milligram protein per 5 minutes, uptake was significantly inhibited by betaine, beta-alanine, nipecotic acid, taurine and quinidine whereas probenecid, L-proline, creatine and glycine had no effect, and confocal immunofluorescent microscopy demonstrated colocalization of GAT2/BGT-1 with P-glycoprotein, a barrier-specific marker, on brain capillaries.

    The GABA transporter GAT2 / BGT-1 → Gamma-aminobutyric acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/11598501.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708", "start_char": 0, "end_char": 1589, "text_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708"}
    experimental_model
    Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line
    exposure
    Tritiated GABA uptake by a conditionally immortalised mouse brain capillary endothelial cell line used as an in vitro barrier model
    limitations
    An in vitro barrier model. It identifies the transporter and its kinetics; it does not establish the direction of net flux across an intact barrier.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Mouse
    plain_language
    The barrier has a dedicated carrier for this molecule, and its affinity is low enough that it only moves appreciable amounts at high concentrations.
    primary_references
    [gb-p11598501] GAT2/BGT-1 as a system responsible for the transport of gamma-aminobutyric acid at the mouse blood-brain barrier. (2001). https://pubmed.ncbi.nlm.nih.gov/11598501/ DOI: 10.1097/00004647-200110000-00012
    tissue_or_cell_type
    Brain capillary endothelium
    transport_effect
    raises Measured as cellular uptake of tritiated GABA, sodium- and chloride-dependent.
    transport_pool
    the expressing cell Measured as cellular uptake of tritiated GABA, sodium- and chloride-dependent.

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 326–337

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line · source_derived_draft · unverified_draft

    ### gb-a-transporter-handles-gaba-at-the-barrier GABA transport was studied by cellular uptake of tritiated GABA which was sodium-, chloride- and concentration-dependent with a Michaelis-Menten constant of 679 plus or minus 80 micromol per litre and a maximal uptake rate of 4,790 pmol per milligram protein per 5 minutes, uptake was significantly inhibited by betaine, beta-alanine, nipecotic acid, taurine and quinidine whereas probenecid, L-proline, creatine and glycine had no effect, and confocal immunofluorescent microscopy demonstrated colocalization of GAT2/BGT-1 with P-glycoprotein, a barrier-specific marker, on brain capillaries. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The barrier has a dedicated carrier for this molecule, and its affinity is low enough that it only moves appreciable amounts at high concentrations. organism: Mouse tissue_or_cell_type: Brain capillary endothelium experimental_model: Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line limitations: An in vitro barrier model. It identifies the transporter and its kinetics; it does not establish the direction of net flux across an intact barrier. exposure: Tritiated GABA uptake by a conditionally immortalised mouse brain capillary endothelial cell line used as an in vitro barrier model evidence_span: {"source_cache": "artifacts/gaba-research/11598501.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708", "start_char": 0, "end_char": 1589, "text_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708"} [gb-p11598501] GAT2/BGT-1 as a system responsible for the transport of gamma-aminobutyric acid at the mouse blood-brain barrier. (2001). https://pubmed.ncbi.nlm.nih.gov/11598501/ DOI: 10.1097/00004647-200110000-00012
    Complete structured claim and evidence

  2. Study of brain to blood efflux transport of carbon-14 GABA after loading the brain by vascular perfusion revealed that the half-time of elimination was significantly shorter in spontaneously hypertensive rats at 5.35 plus or minus 0.66 minutes than in Wistar Kyoto rats at 14.83 plus or minus 1.94 minutes, the faster efflux might at least partially compensate for increased uptake and preserve the protective function of the barrier towards GABA, and systemic infusion of GABA within a wide range of administered doses from 0.004 to 5.00 milligrams per kilogram produced an increase in cerebrospinal fluid GABA concentration from around 0.5 micromolar to only 11 micromolar.

    Brain-to-blood efflux transport of GABA → Cerebrospinal fluid GABA concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/16616765.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550c910f870ffc48b56fbcfe95555a4fec6441bdbef7b1369ef79d1bcba6df5d", "start_char": 0, "end_char": 1941, "text_sha256": "550c910f870ffc48b56fbcfe95555a4fec6441bdbef7b1369ef79d1bcba6df5d"}
    experimental_model
    In situ brain perfusion with efflux measurement and cerebrospinal fluid sampling across a range of systemic doses
    exposure
    Carbon-14 GABA by bilateral in situ brain perfusion, and systemic GABA infusion from 0.004 to 5.00 milligrams per kilogram
    limitations
    Anaesthetised rats, and the comparison is between hypertensive and normotensive strains. The dose-ranging cerebrospinal fluid measurement is the part that bears on oral supplementation.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Rat
    plain_language
    The brain actively pumps this molecule back out, and flooding the bloodstream with it barely shifts the concentration inside.
    primary_references
    [gb-p16616765] Increased brain uptake and brain to blood efflux transport of 14C-GABA in spontaneously hypertensive rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16616765/ DOI: 10.1016/j.lfs.2006.02.039
    tissue_or_cell_type
    Brain, cerebrospinal fluid and cerebral capillaries

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 339–350

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In situ brain perfusion with efflux measurement and cerebrospinal fluid sampling across a range of systemic doses · source_derived_draft · unverified_draft

    ### gb-the-brain-pushes-gaba-back-out Study of brain to blood efflux transport of carbon-14 GABA after loading the brain by vascular perfusion revealed that the half-time of elimination was significantly shorter in spontaneously hypertensive rats at 5.35 plus or minus 0.66 minutes than in Wistar Kyoto rats at 14.83 plus or minus 1.94 minutes, the faster efflux might at least partially compensate for increased uptake and preserve the protective function of the barrier towards GABA, and systemic infusion of GABA within a wide range of administered doses from 0.004 to 5.00 milligrams per kilogram produced an increase in cerebrospinal fluid GABA concentration from around 0.5 micromolar to only 11 micromolar. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The brain actively pumps this molecule back out, and flooding the bloodstream with it barely shifts the concentration inside. organism: Rat tissue_or_cell_type: Brain, cerebrospinal fluid and cerebral capillaries experimental_model: In situ brain perfusion with efflux measurement and cerebrospinal fluid sampling across a range of systemic doses limitations: Anaesthetised rats, and the comparison is between hypertensive and normotensive strains. The dose-ranging cerebrospinal fluid measurement is the part that bears on oral supplementation. exposure: Carbon-14 GABA by bilateral in situ brain perfusion, and systemic GABA infusion from 0.004 to 5.00 milligrams per kilogram evidence_span: {"source_cache": "artifacts/gaba-research/16616765.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550c910f870ffc48b56fbcfe95555a4fec6441bdbef7b1369ef79d1bcba6df5d", "start_char": 0, "end_char": 1941, "text_sha256": "550c910f870ffc48b56fbcfe95555a4fec6441bdbef7b1369ef79d1bcba6df5d"} [gb-p16616765] Increased brain uptake and brain to blood efflux transport of 14C-GABA in spontaneously hypertensive rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16616765/ DOI: 10.1016/j.lfs.2006.02.039
    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.

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