Component
Experimental TRPM8 knockout mouse genotype
Experimental TRPM8 knockout mouse genotype. 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
TRPM8 ablation had no effect on total electromyographic muscle activity, on tachycardia, or on the drop in core temperature during cold exposure, with vehicle, compound 5 and TRPM8 knockout values closely similar across all three measures.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dihydrocapsaicin-research/24005250.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e9d99ac4cc7a031474975ac4d7f3bcff0df922dc01047fe94bd51817ef5b3fea", "start_char": 0, "end_char": 1963, "text_sha256": "e9d99ac4cc7a031474975ac4d7f3bcff0df922dc01047fe94bd51817ef5b3fea"}
- experimental_model
- Conscious mice exposed to 10 degree cooling with implanted electromyography electrodes, electrocardiography and abdominal temperature transmitters
- exposure
- TRPV1 agonist dihydrocapsaicin or TRPM8 inhibitor compound 5, with TRPM8 knockout mice as a control
- limitations
- This is the record that explains why the drug is clinically interesting rather than merely cooling: it removes the defence that makes physical cooling intolerable in a conscious patient.
- nutrient_topic
- Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
- organism
- Mouse
- plain_language
- Deleting the cold receptor changed nothing about the body’s answer to cold.
- primary_references
- [dhc-p24005250] Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition. (2013). https://pubmed.ncbi.nlm.nih.gov/24005250/ DOI: 10.1152/ajpregu.00296.2013
- tissue_or_cell_type
- Back muscle, heart and core
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conscious mice exposed to 10 degree cooling with implanted electromyography electrodes, electrocardiography and abdominal temperature transmitters · source_derived_draft · unverified_draft
### dhc-trpm8-ablation-does-nothing TRPM8 ablation had no effect on total electromyographic muscle activity, on tachycardia, or on the drop in core temperature during cold exposure, with vehicle, compound 5 and TRPM8 knockout values closely similar across all three measures. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Deleting the cold receptor changed nothing about the body’s answer to cold. organism: Mouse tissue_or_cell_type: Back muscle, heart and core experimental_model: Conscious mice exposed to 10 degree cooling with implanted electromyography electrodes, electrocardiography and abdominal temperature transmitters limitations: This is the record that explains why the drug is clinically interesting rather than merely cooling: it removes the defence that makes physical cooling intolerable in a conscious patient. exposure: TRPV1 agonist dihydrocapsaicin or TRPM8 inhibitor compound 5, with TRPM8 knockout mice as a control evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24005250.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e9d99ac4cc7a031474975ac4d7f3bcff0df922dc01047fe94bd51817ef5b3fea", "start_char": 0, "end_char": 1963, "text_sha256": "e9d99ac4cc7a031474975ac4d7f3bcff0df922dc01047fe94bd51817ef5b3fea"} [dhc-p24005250] Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition. (2013). https://pubmed.ncbi.nlm.nih.gov/24005250/ DOI: 10.1152/ajpregu.00296.2013
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.