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

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Abstract

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

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Funding

Center for Neuroplasticity and Pain (CNAP) is supported by the Danish National Research Foundation (DNRF121).

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Authors and Affiliations

  1. Laboratory for Experimental Cutaneous Pain and Itch Research, SMI, Department of Health Science and Technology, Center for Neuroplasticity and Pain, Faculty of Medicine, Aalborg University, Fredrik Bajers Vej 7D, 9220, Aalborg, Denmark

    Silvia Lo Vecchio, Hjalte Holm Andersen & Lars Arendt-Nielsen

  2. Department of Dermato-Allergology, The Allergy Clinic, Copenhagen University Hospital, Gentofte, Copenhagen, Denmark

    Jesper Elberling

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  1. Silvia Lo Vecchio
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  2. Hjalte Holm Andersen
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  3. Jesper Elberling
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  4. Lars Arendt-Nielsen
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HHA and LAN conceived the research idea and designed the study. SLV collected and analyzed the data and wrote the initial manuscript draft.

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Correspondence to Silvia Lo Vecchio.

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Lo Vecchio, S., Andersen, H.H., Elberling, J. et al. Sensory defunctionalization induced by 8% topical capsaicin treatment in a model of ultraviolet-B-induced cutaneous hyperalgesia. Exp Brain Res 239, 2873–2886 (2021). https://doi.org/10.1007/s00221-021-06170-0

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