ArticleCephalalgia : an international journal of headache2025
Prolactin-induced sensitization of trigeminal nociceptors promotes migraine co-morbidity in endometriosis.
Article in Cephalalgia : an international journal of headache, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07519343 (Investigating the inFluence of EndoMetriosis IN migraINE - FEMININE Study), which is not on this map. Cited by 4 papers.
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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.
Investigating the inFluence of EndoMetriosis IN migraINE - FEMININE Study
Who cites it
4 citing papers in PubMed.
- Comparative Electrophysiological Analysis of Trigeminal and Dorsal Root Ganglion Neurons in Mice.eNeuro · 2026Article
- The therapeutic pipeline in migraine: What does the future hold?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Identification of common genetic and molecular signatures in migraine and comorbid conditions.The journal of headache and pain · 2026Review
- Spinal glial cell derived extra-pituitary prolactin contributes to postoperative pain in females.Frontiers in aging neuroscience · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundWomen with endometriosis are more likely to have migraine. The mechanisms underlying this co-morbidity are unknown. Prolactin, a neurohormone secreted and released into circulation from the anterior pituitary, can sensitize sensory neurons from female, but not male, rodents, monkeys and human donors.
methodsWe used a syngeneic model of endometriosis to determine whether elevated prolactin levels can sensitize trigeminal ganglion neurons and increase vulnerability to migraine pain.
resultsMice with endometriotic lesions showed increased serum prolactin levels and developed persistent abdominal, but not cephalic, allodynia. However, inhalation of a transient receptor potential ankyrin 1 agonist, umbellulone, a known environmental trigger of headache in some patients, elicited cephalic allodynia in mice with endometriosis but not sham controls, suggesting that endometriosis can promote sensitization of trigeminal neurons and migraine attacks. Endometriosis dysregulated the expression of prolactin receptor isoforms in trigeminal neurons and increased their excitability measured by
conclusionsThese data demonstrate that circulating prolactin in endometriosis promotes vulnerability to migraine through sensitization of trigeminal afferents. Clinically available dopamine receptor agonists or novel monoclonal antibodies targeting prolactin signaling may be effective for migraine prevention in women with endometriosis.
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