Component

GABA-A receptor delta subunit / GABRD

GABA-A receptor delta subunit / GABRD. Species, exposure and limitations are retained in each linked claim.

3 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. A subset of GABA-A receptor subunits are expressed by CD4-positive T cells including the delta subunit that confers high affinity for GABA and sensitivity to alcohol, GABA at relatively low concentrations down-regulated effector T cell responses to beta cell antigens ex vivo and administration of GABA retarded the adoptive transfer of type 1 diabetes in NOD/scid mice, treatment with a low dose of GABA at 600 micrograms daily dramatically inhibited the development of proinflammatory T cell responses and disease progression in disease-prone mice that already had established autoimmunity, and GABA inhibited T cell receptor-mediated T cell cycle progression in vitro which may underlie the therapeutic effects.

    Gamma-aminobutyric acid → Type 1 diabetes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/15470076.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09", "start_char": 0, "end_char": 1443, "text_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09"}
    experimental_model
    Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice
    exposure
    GABA at low concentrations ex vivo, and 600 micrograms daily in mice with established autoimmunity
    limitations
    A mouse type 1 diabetes model. The cell cycle result offers a mechanism for the disease effect but is measured separately from it.
    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
    Low doses slowed the immune attack on the insulin-producing cells even after that attack had already started.
    primary_references
    [gb-p15470076] Gamma-aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model. (2004). https://pubmed.ncbi.nlm.nih.gov/15470076/ DOI: 10.4049/jimmunol.173.8.5298
    tissue_or_cell_type
    CD4 T cell and pancreatic islet

    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 534–545

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice · source_derived_draft · unverified_draft

    ### gb-gaba-slows-the-autoimmune-t-cell A subset of GABA-A receptor subunits are expressed by CD4-positive T cells including the delta subunit that confers high affinity for GABA and sensitivity to alcohol, GABA at relatively low concentrations down-regulated effector T cell responses to beta cell antigens ex vivo and administration of GABA retarded the adoptive transfer of type 1 diabetes in NOD/scid mice, treatment with a low dose of GABA at 600 micrograms daily dramatically inhibited the development of proinflammatory T cell responses and disease progression in disease-prone mice that already had established autoimmunity, and GABA inhibited T cell receptor-mediated T cell cycle progression in vitro which may underlie the therapeutic effects. 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: Low doses slowed the immune attack on the insulin-producing cells even after that attack had already started. organism: Mouse tissue_or_cell_type: CD4 T cell and pancreatic islet experimental_model: Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice limitations: A mouse type 1 diabetes model. The cell cycle result offers a mechanism for the disease effect but is measured separately from it. exposure: GABA at low concentrations ex vivo, and 600 micrograms daily in mice with established autoimmunity evidence_span: {"source_cache": "artifacts/gaba-research/15470076.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09", "start_char": 0, "end_char": 1443, "text_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09"} [gb-p15470076] Gamma-aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model. (2004). https://pubmed.ncbi.nlm.nih.gov/15470076/ DOI: 10.4049/jimmunol.173.8.5298
    Complete structured claim and evidence

  2. A naturally occurring GABA-A receptor subunit partnership was identified with high sensitivity to ethanol.

    Ethanol → Tonic GABA-A receptor current source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/17159992.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fbee66c99566521e71ae6b95b34c77426888dd791b27b2e3dad3a215a12441f7", "start_char": 0, "end_char": 1048, "text_sha256": "fbee66c99566521e71ae6b95b34c77426888dd791b27b2e3dad3a215a12441f7"}
    experimental_model
    Recombinant GABA-A receptor subunit combinations tested for ethanol sensitivity
    exposure
    Ethanol at low millimolar concentrations on defined subunit partnerships
    limitations
    Identifies a subunit combination sensitive at drinking-relevant concentrations, which had been the main objection to GABA-A as a direct target.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Recombinant human and rodent subunits
    plain_language
    A specific combination of receptor parts responds to alcohol at the concentrations drinking produces.
    primary_references
    [alcohol-p17159992] A new naturally occurring GABA(A) receptor subunit partnership with high sensitivity to ethanol. (2007). https://pubmed.ncbi.nlm.nih.gov/17159992/ DOI: 10.1038/nn1813
    tissue_or_cell_type
    Extrasynaptic GABA-A receptors

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 319–330

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant GABA-A receptor subunit combinations tested for ethanol sensitivity · source_derived_draft · unverified_draft

    ### alcohol-gaba-subunit-sensitivity A naturally occurring GABA-A receptor subunit partnership was identified with high sensitivity to ethanol. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: A specific combination of receptor parts responds to alcohol at the concentrations drinking produces. organism: Recombinant human and rodent subunits tissue_or_cell_type: Extrasynaptic GABA-A receptors experimental_model: Recombinant GABA-A receptor subunit combinations tested for ethanol sensitivity limitations: Identifies a subunit combination sensitive at drinking-relevant concentrations, which had been the main objection to GABA-A as a direct target. exposure: Ethanol at low millimolar concentrations on defined subunit partnerships evidence_span: {"source_cache": "artifacts/alcohol-research/17159992.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fbee66c99566521e71ae6b95b34c77426888dd791b27b2e3dad3a215a12441f7", "start_char": 0, "end_char": 1048, "text_sha256": "fbee66c99566521e71ae6b95b34c77426888dd791b27b2e3dad3a215a12441f7"} [alcohol-p17159992] A new naturally occurring GABA(A) receptor subunit partnership with high sensitivity to ethanol. (2007). https://pubmed.ncbi.nlm.nih.gov/17159992/ DOI: 10.1038/nn1813
    Complete structured claim and evidence

  3. GABA-A receptor delta subunit knockout mice have multiple defects in behavioural responses to ethanol.

    Experimental GABA-A delta subunit knockout mouse genotype → Tonic GABA-A receptor current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/11781502.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9aa25b5b0c1c81f09205b27cbe518898225af41cd3d7e9a948db66619311ca0b", "start_char": 0, "end_char": 1079, "text_sha256": "9aa25b5b0c1c81f09205b27cbe518898225af41cd3d7e9a948db66619311ca0b"}
    experimental_model
    GABA-A delta subunit knockout mice across behavioural ethanol assays
    exposure
    Ethanol behavioural responses in delta-subunit-null mice
    limitations
    A genetic test of the extrasynaptic receptor. Multiple behavioural defects are reported, so the subunit is not specific to one ethanol effect.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Mouse
    plain_language
    Delete the subunit and the animal responds to alcohol differently across several tests.
    primary_references
    [alcohol-p11781502] GABA(A)-receptor delta subunit knockout mice have multiple defects in behavioral responses to ethanol. (2001). https://pubmed.ncbi.nlm.nih.gov/11781502/ DOI: 10.1097/00000374-200112000-00003
    tissue_or_cell_type
    Brain
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 332–343

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GABA-A delta subunit knockout mice across behavioural ethanol assays · source_derived_draft · unverified_draft

    ### alcohol-gabrd-null-behaviour GABA-A receptor delta subunit knockout mice have multiple defects in behavioural responses to ethanol. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Delete the subunit and the animal responds to alcohol differently across several tests. organism: Mouse tissue_or_cell_type: Brain experimental_model: GABA-A delta subunit knockout mice across behavioural ethanol assays limitations: A genetic test of the extrasynaptic receptor. Multiple behavioural defects are reported, so the subunit is not specific to one ethanol effect. exposure: Ethanol behavioural responses in delta-subunit-null mice evidence_span: {"source_cache": "artifacts/alcohol-research/11781502.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9aa25b5b0c1c81f09205b27cbe518898225af41cd3d7e9a948db66619311ca0b", "start_char": 0, "end_char": 1079, "text_sha256": "9aa25b5b0c1c81f09205b27cbe518898225af41cd3d7e9a948db66619311ca0b"} [alcohol-p11781502] GABA(A)-receptor delta subunit knockout mice have multiple defects in behavioral responses to ethanol. (2001). https://pubmed.ncbi.nlm.nih.gov/11781502/ DOI: 10.1097/00000374-200112000-00003
    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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