Component

Tactile allodynia after peripheral nerve injury

Tactile allodynia after peripheral nerve injury. Species, exposure and limitations are retained in each linked claim.

1 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. ATP-stimulated microglia cause a depolarizing shift in the anion reversal potential in spinal lamina I neurons which inverts the polarity of currents activated by GABA as occurs after peripheral nerve injury, applying brain-derived neurotrophic factor mimics the alteration, blocking signalling between BDNF and the receptor TrkB reverses the allodynia and the shift that follows both nerve injury and administration of ATP-stimulated microglia, and preventing BDNF release from microglia by pretreating them with interfering RNA before ATP stimulation also inhibits the effects on the withdrawal threshold.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/gaba-research/16355225.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75e8e0a216ad3cbd68087f650d263b38fe34b73a6b3b253b929b2af26434e001", "start_char": 0, "end_char": 1571, "text_sha256": "75e8e0a216ad3cbd68087f650d263b38fe34b73a6b3b253b929b2af26434e001"}
    experimental_model
    Recordings from lamina I neurons exposed to ATP-stimulated microglia, with BDNF blockade and interfering RNA
    exposure
    ATP-stimulated microglia, applied BDNF, BDNF-TrkB blockade, and interfering RNA against BDNF in microglia
    limitations
    Each link in the chain is cut separately, which is what makes the assignment to BDNF strong. It remains a rodent model of one pain state.
    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
    An immune cell in the spinal cord releases a growth factor that turns the brake into an accelerator.
    primary_references
    [gb-p16355225] BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain. (2005). https://pubmed.ncbi.nlm.nih.gov/16355225/ DOI: 10.1038/nature04223
    tissue_or_cell_type
    Spinal lamina I dorsal horn neuron and microglia
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    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 222–233

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recordings from lamina I neurons exposed to ATP-stimulated microglia, with BDNF blockade and interfering RNA · source_derived_draft · unverified_draft

    ### gb-microglia-invert-the-current ATP-stimulated microglia cause a depolarizing shift in the anion reversal potential in spinal lamina I neurons which inverts the polarity of currents activated by GABA as occurs after peripheral nerve injury, applying brain-derived neurotrophic factor mimics the alteration, blocking signalling between BDNF and the receptor TrkB reverses the allodynia and the shift that follows both nerve injury and administration of ATP-stimulated microglia, and preventing BDNF release from microglia by pretreating them with interfering RNA before ATP stimulation also inhibits the effects on the withdrawal threshold. Condition category: machinery_impairment 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: An immune cell in the spinal cord releases a growth factor that turns the brake into an accelerator. organism: Rat tissue_or_cell_type: Spinal lamina I dorsal horn neuron and microglia experimental_model: Recordings from lamina I neurons exposed to ATP-stimulated microglia, with BDNF blockade and interfering RNA limitations: Each link in the chain is cut separately, which is what makes the assignment to BDNF strong. It remains a rodent model of one pain state. exposure: ATP-stimulated microglia, applied BDNF, BDNF-TrkB blockade, and interfering RNA against BDNF in microglia evidence_span: {"source_cache": "artifacts/gaba-research/16355225.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75e8e0a216ad3cbd68087f650d263b38fe34b73a6b3b253b929b2af26434e001", "start_char": 0, "end_char": 1571, "text_sha256": "75e8e0a216ad3cbd68087f650d263b38fe34b73a6b3b253b929b2af26434e001"} [gb-p16355225] BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain. (2005). https://pubmed.ncbi.nlm.nih.gov/16355225/ DOI: 10.1038/nature04223
    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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