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Abstract

The development of chronic pain is typically predicated by neuroplastic changes within the spinal cord in response to persistent noxious stimuli, termed central sensitization. Sensitization increases the sensitivity to stimuli of neurons directly in contact with the initial noxious stimulus, termed primary hyperalgesia, as well as those in the adjacent regions, termed secondary hyperalgesia. TRPV1 receptors, found throughout the spinal cord and periphery, are key contributors to the development t of sensitization. Capsaicin, the active ingredient in chili peppers, is a known agonist of TRPV1 receptors and, due to the unique ability of these receptors to become defunctionalized with intense or prolonged capsaicin exposure, is a common ingredient in pain relieving ointments. Defunctionalization, via capsaicin, eliminates the typical primary sensitization and has been demonstrated through the application of high dosage (>5%) capsaicin treatments. The purpose of this study was to analyze the effects of defunctionalizing capsaicin-sensitive nociceptors, using a prolonged low concentration (