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Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain
Open accessAbstract
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.
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“The prolactin-PRLR axis contributes to the activation of pain-related pathways through the sensitization of transient receptor potential channels that promote painful sensations [157,158].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [157]
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Metadata
- Authors
- Patil, M. J., Ruparel, S. B., Henry, M. A., & Akopian, A. N.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Akopian, Armen N.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2013-11-01
- Volume
- 305
- Issue
- 9
- Pages
- E1154-E1164
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- PMC
- PMC3840203
- OpenAlex
- W2048163077
- Cited by
- 90
- References
- 77
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 5 · 2023: 12 · 2022: 5 · 2021: 13 · 2020: 11 · 2019: 9 · 2018: 4 · 2017: 5 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 1
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM112747)
- National Institute of Dental and Craniofacial Research (R01DE017696)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- prolactin, prolactin receptor, TRPV1, TRPA1, TRPM8, TRP channels, sensory neurons, sex differences, inflammatory pain, hyperalgesia, mechanical allodynia, cold hyperalgesia, dorsal root ganglia, complete Freund's adjuvant, peripheral sensitization
- MeSH terms
- TRPA1 Cation Channel, Animals, Behavior, Animal, Cold Temperature, Female, Ganglia, Spinal, Hot Temperature, Hyperalgesia, Inflammation, Male, Nociceptors, Pain, Physical Stimulation, Prolactin, Receptors, Prolactin, Sensory Receptor Cells, Sex Characteristics, Rats, Sprague-Dawley, Mice, Knockout, TRPC Cation Channels, TRPM Cation Channels, TRPV Cation Channels, Mice, Rats, Real-Time Polymerase Chain Reaction
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