ArticleThe Journal of biological chemistry2013
Mechanisms of transient signaling via short and long prolactin receptor isoforms in female and male sensory neurons.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Prolactin and pain of endometriosis.Pharmacology & therapeutics · 2023Pooled it
- Kinetics of cell-free DNA in response to exogenous and exertional heating in healthy young men.European journal of applied physiology · 2026Trial
- Trial
- Lymphotoxin-beta receptor controls the development of chronic pain.Cell reports · 2026Article
- Spinal glial cell derived extra-pituitary prolactin contributes to postoperative pain in females.Frontiers in aging neuroscience · 2026Article
- Macrophages and iNOS contribute to the effects of dural prolactin and repeated stress in mouse migraine models.The journal of headache and pain · 2025Article
- Dopamine and prolactin in migraine: Mechanisms and potential therapeutic targets.Journal of neuroendocrinology · 2025Review
- Identification of sensory fiber types in mouse temporomandibular joint tissues.Scientific reports · 2025Article
- 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 · 2025Article
- Prolactin-induced sensitization of trigeminal nociceptors promotes migraine co-morbidity in endometriosis.Cephalalgia : an international journal of headache · 2025Article
- Prolactin and Hyperprolactinaemia in Endometriosis-Related Infertility: Are There Clinically Significant Connections?Journal of clinical medicine · 2024Review
- Female-selective mechanisms promoting migraine.The journal of headache and pain · 2024Review
- Sensory innervation of masseter, temporal and lateral pterygoid muscles in common marmosets.Scientific reports · 2023Article
- Prolactin and oxytocin: potential targets for migraine treatment.The journal of headache and pain · 2023Review
- The brain as a source and a target of prolactin in mammals.Neural regeneration research · 2022Review
- Unveiling the Pathogenesis of Adenomyosis through Animal Models.Journal of clinical medicine · 2022Review
- A prolactin-dependent sexually dimorphic mechanism of migraine chronification.Cephalalgia : an international journal of headache · 2022Article
- Sex-dependent pain trajectories induced by prolactin require an inflammatory response for pain resolution.Brain, behavior, and immunity · 2022Article
- A link between migraine and prolactin: the way forward.Future science OA · 2021Review
- Pituitary hormones are specifically expressed in trigeminal sensory neurons and contribute to pain responses in the trigeminal system.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Prolactin (PRL) regulates activity of nociceptors and causes hyperalgesia in pain conditions. PRL enhances nociceptive responses by rapidly modulating channels in nociceptors. The molecular mechanisms underlying PRL-induced transient signaling in neurons are not well understood. Here we use a variety of cell biology and pharmacological approaches to show that PRL transiently enhanced capsaicin-evoked responses involve protein kinase C ε (PKCε) or phosphatidylinositol 3-kinase (PI3K) pathways in female rat trigeminal (TG) neurons. We next reconstituted PRL-induced signaling in a heterologous expression system and TG neurons from PRL receptor (PRLR)-null mutant mice by expressing rat PRLR-long isoform (PRLR-L), PRLR-short isoform (PRLR-S), or a mix of both. Results show that PRLR-S, but not PRLR-L, is capable of mediating PRL-induced transient enhancement of capsaicin responses in both male and female TG neurons. However, co-expression of PRLR-L with PRLR-S (1:1 ratio) leads to the inhibition of the transient PRL actions. Co-expression of PRLR-L deletion mutants with PRLR-S indicated that the cytoplasmic site adjacent to the trans-membrane domain of PRLR-L was responsible for inhibitory effects of PRLR-L. Furthermore, in situ hybridization and immunohistochemistry data indicate that in normal conditions, PRLR-L is expressed mainly in glia with little expression in rat sensory neurons (3-5%) and human nerves. The predominant PRLR form in TG neurons/nerves from rats and humans is PRLR-S. Altogether, PRL-induced transient signaling in sensory neurons is governed by PI3K or PKCε, mediated via the PRLR-S isoform, and transient effects mediated by PRLR-S are inhibited by presence of PRLR-L in these cells.
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Registered trials
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.