Evidence map›Paper›PMID 35968676›Full record

ArticleeLife2022

TRPV1 drugs alter core body temperature via central projections of primary afferent sensory neurons.

Wendy Wing Sze Yue, Lin Yuan, Joao M Braz, Allan I Basbaum, David Julius

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  17. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
  18. TRP Channels in Stroke.Neuroscience bulletin · 2024
    Review
  19. TRPV1 Channels in the Central Nervous System as Drug Targets.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Wendy Wing Sze YueDepartment of Physiology, University of California, San Francisco, United States.ORCID 0000-0002-7736-4262
Lin YuanDepartment of Physiology, University of California, San Francisco, United States.
Joao M BrazDepartment of Anatomy, University of California, San Francisco, United States.
Allan I BasbaumDepartment of Anatomy, University of California, San Francisco, United States.
David JuliusDepartment of Physiology, University of California, San Francisco, United States.ORCID 0000-0002-6365-4867
University of California, San Francisco · US

Funding

Natural products as probes of the pain pathwayR35NS105038 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JULIUS, DAVID · 2018 to 2025
$9.0M
From the spinal cord to the brain: Neurology of the pain and itch neuronsR35NS097306 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASBAUM, ALLAN I. · 2017 to 2024
$7.2M
Howard Hughes Medical InstituteNINDS NIH HHS R35 NS097306NINDS NIH HHS R35 NS105038
6 · The paper itself

Abstract

TRPV1, a capsaicin- and heat-activated ion channel, is expressed by peripheral nociceptors and has been implicated in various inflammatory and neuropathic pain conditions. Although pharmacological modulation of TRPV1 has attracted therapeutic interest, many TRPV1 agonists and antagonists produce thermomodulatory side effects in animal models and human clinical trials, limiting their utility. These on-target effects may result from the perturbation of TRPV1 receptors on nociceptors, which transduce signals to central thermoregulatory circuits and release proinflammatory factors from their peripheral terminals, most notably the potent vasodilative neuropeptide, calcitonin gene-related peptide (CGRP). Alternatively, these body temperature effects may originate from the modulation of TRPV1 on vascular smooth muscle cells (vSMCs), where channel activation promotes arteriole constriction. Here, we ask which of these pathways is most responsible for the body temperature perturbations elicited by TRPV1 drugs in vivo. We address this question by selectively eliminating TRPV1 expression in sensory neurons or vSMCs and show that only the former abrogates agonist-induced hypothermia and antagonist-induced hyperthermia. Furthermore, lesioning the central projections of TRPV1-positive sensory nerve fibers also abrogates drug-mediated thermomodulation, whereas eliminating CGRP has no effect. Thus, TRPV1 drugs alter core body temperature by modulating sensory input to the central nervous system, rather than through peripheral actions on the vasculature. These findings suggest how mechanistically distinct TRPV1 antagonists may diminish inflammatory pain without affecting core body temperature.

Indexed as

Body TemperatureNeuralgiaAnimalsCalcitonin Gene-Related PeptideCapsaicinHumansSensory Receptor CellsTRPV Cation ChannelsCalcitonin Gene-Related PeptideCapsaicinTRPV1 protein, humanTRPV Cation ChannelsCGRPmouseneurosciencesensory neuronsthermoregulationTRPV1

Identifiers

PMID35968676
PMCPMC9377796
OpenAlexW4291511692

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.