Component
Brain-derived neurotrophic factor
Brain-derived neurotrophic factor. 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.