Evidence map›Paper›PMID 24022869›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain.

Mayur J Patil, Shivani B Ruparel, Michael A Henry, Armen N Akopian

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 21% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Prolactin and pain of endometriosis.Pharmacology & therapeutics · 2023
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. A prolactin-targeting antibody to prevent stress-induced peripheral nociceptor sensitization and female postoperative pain.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Mayur J PatilDepartment of Pharmacology University of Texas Health Science Center at San Antonio, San Antonio, Texas; and.
Shivani B Ruparel
Michael A Henry
Armen N Akopian
The University of Texas Health Science Center at San Antonio · US

Funding

Prolactin Regulation of Trigeminal NociceptorsR01DE017696 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AKOPIAN, ARMEN N · 2007 to 2011
$1.8M
Prolactin regulation of postoperative pain in males and femalesR01GM112747 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AKOPIAN, ARMEN N · 2015 to 2018
$1.2M
NIDCR NIH HHS R01-DE-017696NIGMS NIH HHS R01 GM112747
6 · The paper itself

Abstract

Prolactin (PRL) is a hormone produced in the anterior pituitary but also synthesized extrapituitary where it can influence diverse cellular processes, including inflammatory responses. Females experience greater pain in certain inflammatory conditions, but the contribution of the PRL system to sex-dependent inflammatory pain is unknown. We found that PRL regulates transient receptor potential (TRP) channels in a sex-dependent manner in sensory neurons. At >20 ng/ml, PRL sensitizes TRPV1 in female, but not male, neurons. This effect is mediated by PRL receptor (PRL-R). Likewise, TRPA1 and TRPM8 were sensitized by 100 ng/ml PRL only in female neurons. We showed that complete Freund adjuvant (CFA) upregulated PRL levels in the inflamed paw of both male and female rats, but levels were higher in females. In contrast, CFA did not change mRNA levels of long and short PRL-R in the dorsal root ganglion or spinal cord. Analysis of PRL and PRL-R knockout (KO) mice demonstrated that basal responses to cold stimuli were only altered in females, and with no significant effects on heat and mechanical responses in both sexes. CFA-induced heat and cold hyperalgesia were not changed in PRL and PRL-R KO compared with wild-type (WT) males, whereas significant reduction of heat and cold post-CFA hyperalgesia was detected in PRL and PRL-R KO females. Attenuation of CFA-induced mechanical allodynia was observed in both PRL and PRL-R KO females and males. Thermal hyperalgesia in PRL KO females was restored by administration of PRL into hindpaws. Overall, we demonstrate a sex-dependent regulation of peripheral inflammatory hyperalgesia by the PRL system.

Indexed as

AnimalsBehavior, AnimalCold TemperatureFemaleGanglia, SpinalHot TemperatureHyperalgesiaInflammationMaleMiceMice, KnockoutNociceptorsPainPhysical StimulationProlactinRatsProlactinReceptors, ProlactinTRPA1 Cation ChannelTrpa1 protein, ratTRPC Cation ChannelsTrpm8 protein, ratTRPM Cation ChannelsTrpv1 protein, ratTRPV Cation Channelsfemaleinflammationpainprolactin receptortransient receptor potential A1transient receptor potential M8transient receptor potential V1

Identifiers

PMID24022869
PMCPMC3840203
OpenAlexW2048163077

What OpenQuestion holds

Textmetadata
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.