Component
Peripheral nerve injury
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.
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
Following peripheral nerve injury there is a trans-synaptic reduction in the expression of the potassium-chloride exporter KCC2 and consequent disruption of anion homeostasis in neurons of lamina I of the superficial dorsal horn, the resulting shift in the transmembrane anion gradient caused normally inhibitory anionic synaptic currents to be excitatory, substantially driving up the net excitability of lamina I neurons, and local blockade or knock-down of the spinal KCC2 exporter in intact rats markedly reduced the nociceptive threshold, confirming that the disruption of anion homeostasis was sufficient to cause neuropathic pain.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/gaba-research/12931188.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f465ce014f8ada8e6018e23f0009197609a343241b8d0926b34ed186ce345fa4", "start_char": 0, "end_char": 1073, "text_sha256": "f465ce014f8ada8e6018e23f0009197609a343241b8d0926b34ed186ce345fa4"}
- experimental_model
- Recordings from lamina I neurons after peripheral nerve injury, with spinal blockade and knockdown in intact animals
- exposure
- Peripheral nerve injury, and local blockade or knock-down of spinal KCC2 in intact rats
- limitations
- The knockdown in intact animals is what makes this causal rather than correlative: reproducing the gradient change alone reproduced the pain phenotype.
- 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
- After nerve injury the inhibitory synapses in the pain pathway start doing the opposite of inhibiting.
- primary_references
- [gb-p12931188] Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain. (2003). https://pubmed.ncbi.nlm.nih.gov/12931188/ DOI: 10.1038/nature01868
- tissue_or_cell_type
- Spinal lamina I dorsal horn neuron
- 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 after peripheral nerve injury, with spinal blockade and knockdown in intact animals · source_derived_draft · unverified_draft
### gb-inhibition-becomes-excitation Following peripheral nerve injury there is a trans-synaptic reduction in the expression of the potassium-chloride exporter KCC2 and consequent disruption of anion homeostasis in neurons of lamina I of the superficial dorsal horn, the resulting shift in the transmembrane anion gradient caused normally inhibitory anionic synaptic currents to be excitatory, substantially driving up the net excitability of lamina I neurons, and local blockade or knock-down of the spinal KCC2 exporter in intact rats markedly reduced the nociceptive threshold, confirming that the disruption of anion homeostasis was sufficient to cause neuropathic pain. 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: After nerve injury the inhibitory synapses in the pain pathway start doing the opposite of inhibiting. organism: Rat tissue_or_cell_type: Spinal lamina I dorsal horn neuron experimental_model: Recordings from lamina I neurons after peripheral nerve injury, with spinal blockade and knockdown in intact animals limitations: The knockdown in intact animals is what makes this causal rather than correlative: reproducing the gradient change alone reproduced the pain phenotype. exposure: Peripheral nerve injury, and local blockade or knock-down of spinal KCC2 in intact rats evidence_span: {"source_cache": "artifacts/gaba-research/12931188.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f465ce014f8ada8e6018e23f0009197609a343241b8d0926b34ed186ce345fa4", "start_char": 0, "end_char": 1073, "text_sha256": "f465ce014f8ada8e6018e23f0009197609a343241b8d0926b34ed186ce345fa4"} [gb-p12931188] Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain. (2003). https://pubmed.ncbi.nlm.nih.gov/12931188/ DOI: 10.1038/nature01868
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.