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Maintenance mechanism of nociplastic pain in males

McDonough KE, Hankerd KM, La J-H, Chung JM (2019) Maintenance mechanism of nociplastic pain in males. Neuroscience 2019 Abstracts 218.22. Society for Neuroscience, Chicago, IL.

Summary: Recently, the International Association for the Study of Pain defined a third form of pain: nociplastic pain. A key mechanism of nociplastic pain is central sensitization (CS) persistently maintained in the absence of an underlying persistent injury. We developed a novel mouse model of nociplastic pain, which uses hindpaw capsaicin injection as a transient injury, followed by innocuous vibration stimulation, making CS persist beyond the normal resolution time. Our lab has previously shown that the normally resolving transient CS by capsaicin is maintained by ongoing nerve activity at the injury site in female mice. We preliminarily found that the persistent CS in our male nociplastic pain model is maintained by different mechanisms. Based on the literature that spinal microglia and their inflammatory mediators play a key role in other models of chronic pain, specifically in males, we hypothesize that nociplastic pain in males is due to CS maintained by activated microglia and subsequent release of inflammatory mediators such as prostaglandins generated through the cyclooxygenase (COX) pathway. To test this hypothesis, spinal microglia and COX were inhibited by intrathecally injecting the microglia-targeting toxin Mac-1-saporin or the COX inhibitor indomethacin, respectively, following establishment of a nociplastic pain state. Secondary mechanical hypersensitivity, a behavioral biomarker of CS, was mitigated by intrathecal Mac-1-saporin, whereas intrathecal indomethacin had no effect. Our results suggest that spinal microglia maintain persistent CS driving nociplastic pain in males. However, prostaglandins generated through the COX pathway do not seem to be the main inflammatory mediator involved in the maintenance of this CS.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)