Component

Brain capillary endothelial cells

Brain capillary endothelial cells. Species, exposure and limitations are retained in each linked claim.

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

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.

    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. Gabapentin is a novel anticonvulsant drug with a mechanism of action apparently dissimilar to that of other antiepileptic agents, the detergent-solubilized binding protein from pig cerebral cortex membranes was purified 1022-fold, the purified protein had an apparent subunit molecular weight of 130,000 and was heavily glycosylated, its partial N-terminal amino acid sequence EPFPSAVTIK was identical to that reported for the alpha2delta subunit of the L-type calcium channel, binding to cells transfected with alpha2delta complementary DNA was elevated more than 10-fold over controls, and tritiated gabapentin is the first pharmacological agent described that interacts with an alpha2delta subunit of a voltage-dependent calcium channel.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/8621444.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1723620d459b4f48ad397d59284df3f0619894ba82c6d066a42a47a0edb22216", "start_char": 0, "end_char": 1531, "text_sha256": "1723620d459b4f48ad397d59284df3f0619894ba82c6d066a42a47a0edb22216"}
    experimental_model
    Purification of a radioligand binding protein from pig cerebral cortex with N-terminal sequencing and expression in transfected cells
    exposure
    Tritiated gabapentin binding, followed through a six-step purification to protein identity
    limitations
    A binding and purification study. It identifies what the drug binds; it does not test the GABA receptors, so the absence of GABA-receptor binding is not measured here.
    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
    Pig and rat
    plain_language
    The anticonvulsant designed as a GABA analogue turned out to bind a calcium channel subunit instead.
    primary_references
    [gb-p8621444] The novel anticonvulsant drug, gabapentin (Neurontin), binds to the alpha2delta subunit of a calcium channel. (1996). https://pubmed.ncbi.nlm.nih.gov/8621444/ DOI: 10.1074/jbc.271.10.5768
    tissue_or_cell_type
    Cerebral cortex, heart and skeletal muscle

    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 300–311

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purification of a radioligand binding protein from pig cerebral cortex with N-terminal sequencing and expression in transfected cells · source_derived_draft · unverified_draft

    ### gb-the-drug-named-for-gaba-binds-a-calcium-channel Gabapentin is a novel anticonvulsant drug with a mechanism of action apparently dissimilar to that of other antiepileptic agents, the detergent-solubilized binding protein from pig cerebral cortex membranes was purified 1022-fold, the purified protein had an apparent subunit molecular weight of 130,000 and was heavily glycosylated, its partial N-terminal amino acid sequence EPFPSAVTIK was identical to that reported for the alpha2delta subunit of the L-type calcium channel, binding to cells transfected with alpha2delta complementary DNA was elevated more than 10-fold over controls, and tritiated gabapentin is the first pharmacological agent described that interacts with an alpha2delta subunit of a voltage-dependent calcium channel. 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 anticonvulsant designed as a GABA analogue turned out to bind a calcium channel subunit instead. organism: Pig and rat tissue_or_cell_type: Cerebral cortex, heart and skeletal muscle experimental_model: Purification of a radioligand binding protein from pig cerebral cortex with N-terminal sequencing and expression in transfected cells limitations: A binding and purification study. It identifies what the drug binds; it does not test the GABA receptors, so the absence of GABA-receptor binding is not measured here. exposure: Tritiated gabapentin binding, followed through a six-step purification to protein identity evidence_span: {"source_cache": "artifacts/gaba-research/8621444.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1723620d459b4f48ad397d59284df3f0619894ba82c6d066a42a47a0edb22216", "start_char": 0, "end_char": 1531, "text_sha256": "1723620d459b4f48ad397d59284df3f0619894ba82c6d066a42a47a0edb22216"} [gb-p8621444] The novel anticonvulsant drug, gabapentin (Neurontin), binds to the alpha2delta subunit of a calcium channel. (1996). https://pubmed.ncbi.nlm.nih.gov/8621444/ DOI: 10.1074/jbc.271.10.5768
    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