Experimental TRPV1 knockout mouse genotype: molecular mechanisms & dependencies

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Dihydrocapsaicin at 1.25 mg/kg produced a stable drop in core temperature to 33 degrees in naive and ischaemia-reperfusion mice but not in TRPV1 knockout mice, and had no measurable effect on heart rate or cerebral perfusion while producing a slight transient drop in mean arterial pressure of less than 6 millimetres of mercury.
Dihydrocapsaicin → Hypothermia induced by a drug rather than by physical cooling source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"}
experimental_model
Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion
exposure
Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm
limitations
The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects.
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
The cooling happens through the receptor, and in these mice it barely touched the circulation.
primary_references
[dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
tissue_or_cell_type
Brain and cardiovascular system
trigger_kind
machinery_impairment Imported condition classification; unverified.
Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 296–307
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion · source_derived_draft · unverified_draft
### dhc-hypothermia-requires-trpv1 Dihydrocapsaicin at 1.25 mg/kg produced a stable drop in core temperature to 33 degrees in naive and ischaemia-reperfusion mice but not in TRPV1 knockout mice, and had no measurable effect on heart rate or cerebral perfusion while producing a slight transient drop in mean arterial pressure of less than 6 millimetres of mercury. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The cooling happens through the receptor, and in these mice it barely touched the circulation. organism: Mouse tissue_or_cell_type: Brain and cardiovascular system experimental_model: Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion limitations: The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects. exposure: Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"} [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
Complete structured claim and evidence
In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support.
Hypothermia induced by a drug rather than by physical cooling → Cerebral infarct volume source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"}
experimental_model
Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion
exposure
Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm
limitations
The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects.
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
The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold.
primary_references
[dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
tissue_or_cell_type
Brain and cardiovascular system
trigger_kind
machinery_impairment Imported condition classification; unverified.
Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 309–320
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion · source_derived_draft · unverified_draft
### dhc-infarct-reduction In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold. organism: Mouse tissue_or_cell_type: Brain and cardiovascular system experimental_model: Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion limitations: The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects. exposure: Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"} [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
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Experimental TRPV1 knockout mouse genotype