Peripheral and central neuroplasticity in a mouse model of endometriosis

Joel Castro, Jessica Maddern, Maddern J, Andelain Erickson, Erickson A, Andrea M. Harrington, Stuart M. Brierley
Journal of neurochemistry · 2023 · vol. 168(11) , pp. 3777–3800 · doi:10.1111/jnc.15843 · PMID:37165846 · W4376133484
article OA: hybrid CC0 ⤵ 6 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-06 ⓘ

This study found that endometriosis causes peripheral hypersensitivity of vaginal sensory afferents and central neuroinflammation and sensitization in the spinal cord, explaining increased pain sensitivity.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Chronic pelvic pain (CPP) is the most debilitating symptom of gynaecological disorders such as endometriosis. However, it remains unclear how sensory neurons from pelvic organs affected by endometriosis, such as the female reproductive tract, detect and transmit nociceptive events and how these signals are processed within the central nervous system (CNS). Using a previously characterized mouse model of endometriosis, we investigated whether the increased pain sensitivity occurring in endometriosis could be attributed to (i) changes in mechanosensory properties of sensory afferents innervating the reproductive tract, (ii) alterations in sensory input from reproductive organs to the spinal cord or (iii) neuroinflammation and sensitization of spinal neural circuits. Mechanosensitivity of vagina-innervating primary afferents was examined using an ex vivo single-unit extracellular recording preparation. Nociceptive signalling from the vagina to the spinal cord was quantified by phosphorylated MAP kinase ERK1/2 immunoreactivity. Immunohistochemistry was used to determine glial and neuronal circuit alterations within the spinal cord. We found that sensory afferents innervating the rostral, but not caudal portions of the mouse vagina, developed mechanical hypersensitivity in endometriosis. Nociceptive signalling from the vagina to the spinal cord was significantly enhanced in mice with endometriosis. Moreover, mice with endometriosis developed microgliosis, astrogliosis and enhanced substance P neurokinin-1 receptor immunoreactivity within the spinal cord, suggesting the development of neuroinflammation and sensitization of spinal circuitry in endometriosis. These results demonstrate endometriosis-induced neuroplasticity occurring at both peripheral and central sites of sensory afferent pathways. These findings may help to explain the altered sensitivity to pain in endometriosis and provide a novel platform for targeted pain relief treatments for this debilitating disorder.

My notes (saved in your browser only)

Condition tags

endometriosischronic_pelvic_pain

MeSH descriptors

Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal Disease Models, Animal

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (8)

Source provenance

europepmc
last seen: 2026-08-27T06:11:05.884134+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-08-27T06:10:09.942525+00:00
License: CC0 · commercial use OK