Experimental animal study reveals divergent electrical sensitivity shifts between silent nociceptors and C-touch fibers in pigs, indicating silent nociceptors drive UV-B hyperalgesia.
Introduction: Tetrodotoxin-resistant voltage-sensitive sodium channel subtypes 1.8 and 1.9 play a key role on "silent" (mechano-insensitive) nociceptors activation during sinusoidal electrical stimulation. Therefore, we hypothesized that an UVB-induced sensitization of this particular nociceptor class can be revealed by such electrical stimulation pattern. Objectives: We set out to study ultraviolet-B (UV-B)-induced sensitization of C-nociceptors using heat and mechanical stimulation, but also transduction independent slow depolarizing electrical pulses. Methods: Single fibre recordings of pig saphenous nerve were performed after UV-B irradiation with 3-fold minimum erythemal doses. Results: A total 45 C fibers were recorded from UV-B inflamed skin and discharge patterns compared with nonirradiated control units (n = 134). We did not observe a sensitization to heat or mechanical stimulation in mechanosensitive nociceptors, but some of the "silent" nociceptors were sensitized to mechanical stimulation. The most drastic changes were found for electrical activation thresholds that increased about 3-fold in tactile "C-touch" fibers, but that were reduced in silent nociceptors up to a factor of 5. The threshold to 1-Hz stimulation was also increased 2-fold in "polymodal" nociceptors, although not significantly. Conclusion: 1.8 sodium channels in silent nociceptors. Functionally, sensitized silent nociceptors appear to be the primary candidate to underlie hyperalgesia in acute UV-B inflammation.
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Soares et al. (2026) studied this question.
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