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J Pain. 2013 Jul;14(7):739-46. doi: 10.1016/j.jpain.2013.02.007. Epub 2013 Apr 30.

Modality-specific nociceptor sensitization following UV-B irradiation of human skin.

Author information

1
Department of Anaesthesiology, Medical Faculty Mannheim, University of Heidelberg, Germany.

Abstract

Ultraviolet-B (UV-B) irradiation is a well-established inflammatory pain model inducing mechanical and thermal hyperalgesia, presumably mediated by released mediators that sensitize sensory nerve endings. Here, we used additional electrical stimulation to investigate axonal hyperexcitability. The lower leg of 13 volunteers was irradiated with 3-fold the minimum erythema UV-B dose and sensitization was recorded at days 1, 3, 7, and 14. Maximum heat pain (47°C, 5 seconds) developed at day 1 (visual analog scale [VAS: 0-100]; 59), was reduced at day 3 (VAS 43, P < .002), and was back to normal at day 7 (VAS 18). Mechanical impact pain (8 m/s), pinprick (150 mN), and pressure (100 kPa) hyperalgesia were maximum throughout days 1 to 3 (VAS 16, 8, and 12, respectively, P < .001) and back to normal at day 7. Suprathreshold transcutaneous electrical stimuli (1.5-fold pain threshold) were delivered in trains of 10 pulses at frequencies of 5 to 100 Hz. Electrical pain thresholds (determined at 2 Hz) decreased significantly (P < .002) and suprathreshold electrical pain increased by about 70% at days 1 to 3 after irradiation (VAS 36, P < .002). Electrical hyperalgesia did not correlate with mechanical sensitization but with reduced heat pain threshold and increased tonic heat pain (r = -.46 and .53; P < .05 and < .01), indicating that axonal hyperexcitability might contribute to heat hyperalgesia. Released inflammatory mediators (eg, prostaglandins) might sensitize both heat transducer molecules and axonal ion channels and receptors, which would explain the simultaneous development and close correlation between heat hyperalgesia and axonal hyperexcitability.

PERSPECTIVE:

Local inflammation by UV-B irradiation sensitizes not only sensory endings, but also axons. Increased axonal excitability could contribute to inflammatory hyperalgesia by facilitating spike generation and increasing peak discharge frequencies of nociceptors. Thus, axonal channels and receptors crucial for this sensitization need to be identified to provide new therapeutic targets.

PMID:
23642411
DOI:
10.1016/j.jpain.2013.02.007
[Indexed for MEDLINE]

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