OXYTOCIN MODULATES CENTRAL DESCENDING PAIN PATHWAYS IN A RAT MODEL OF PROVOKED VULVODYNIA

Background: Provoked vulvodynia (PV) is a common chronic genital pain disorder and a leading cause of pelvic pain in women, often resulting in reduced sexual desire and impaired quality of life. Current treatments for PV remain insufficient. Despite growing evidence for oxytocin’s analgesic properties, its role in central pain modulatory circuits remains largely unexplored. Thus, this study aimed to investigate whether oxytocin modulates vulvar hypersensitivity via central pain processing and descending inhibitory pathways in a rat model of PV.
Methods: Female Sprague–Dawley rats (n = 8/group) were subjected to a repeated zymosan induced inflammation model to induce PV. Oxytocin was administered intranasally (16 µg in 50 µL citrate buffer, pH 5.5). Mechanical and thermal sensitivity, anxiety-like behaviour, and sexual motivation were assessed. mRNA expression of genes related to neuroplasticity, neuromodulation, and nociceptive signalling was quantified in key nodes of the pain modulatory network, including the anterior cingulate cortex (ACC), periaqueductal grey (PAG), and rostral ventromedial medulla (RVM).
Results: Intranasal oxytocin significantly attenuated zymosan induced mechanical and thermal hypersensitivity and reduced anxiety-like behaviour, while restoring impairments in sexual motivation. At the molecular level, oxytocin normalized Zymosan induced transcriptional alterations within the ACC, PAG, and RVM, indicating modulation of central pain processing and descending inhibitory pathways.
Conclusions: These findings demonstrate that oxytocin engages central pain modulatory circuits to alleviate chronic vulvar pain. The results highlight oxytocin as a key neuromodulator of brain-behaviour interactions in female chronic pain and provide mechanistic insight into its role in regulating maladaptive pain states.