Sensory defunctionalization induced by 8% topical capsaicin treatment in a model of ultraviolet-B-induced cutaneous hyperalgesia

Subpopulations of primary nociceptors (C- and Aδ-fibers), express the TRPV1 receptor for heat capsaicin. During cutaneous inflammation, these afferents may become sensitized, leading to hyperalgesia. It is known that TRPV1+ are involved in hyperalgesia; however, their involvement mechanical hyperalgesia unclear. This study explored contribution capsaicin-sensitive development humans following ultraviolet-B (UVB) irradiation. Skin areas 18 healthy volunteers were randomized treatment with 8% capsaicin/vehicle patches 24 h. After removal, one capsaicin-treated area vehicle irradiated 2xMED (minimal erythema dose) UVB. 1, 3 7 days post-UVB exposure, tests performed evaluate UVB-induced hyperalgesia: thermal detection pain thresholds, sensitivity supra-threshold stimuli, threshold sensitivity, touch pleasantness, trans-epidermal water loss (TEWL), inflammatory response, pigmentation micro-vascular reactivity. Capsaicin pre-treatment, UVB-irradiated (Capsaicin + UVB area), increased thresholds (P < 0.05), decreased 0.05) irradiation, while resulted unchanged > 0.2). No effects capsaicin reported on pleasantness = 1), TEWL 0.31), response 0.3) or reactivity 0.8) ablation predominantly defunctionalizes TRPV1+-expressing responsible transduction, suggesting sensitization fibers required inflammation but they likely only partially necessary establishment robust