Ultraviolet-B-induced mechanical hyperalgesia: A role for peripheral sensitisation

摘要: Ultraviolet (UV) induced cutaneous inflammation is emerging as a model of pain with novel sensory phenotype. A UVB dose 1000mJ/cm2 produces highly significant thermal and mechanical hypersensitivity. Here we examined the properties mechanisms such hyperalgesia in rats. Significantly, (with approximately 60% change withdrawal thresholds) was restricted to lesion site no changes threshold adjacent non-irradiated skin (i.e. secondary hypersensitivity), suggesting peripheral mechanism. Consistent this, found that primary hypersensitivity showed after intrathecal treatment 10microg NMDA-receptor antagonist MK-801. Using an vitro skin-nerve preparation, presence absence UVB-inflammation, suprathreshold responses displacement stimuli 6-768microm 103 nociceptors were recorded. At peak UVB-induced observed response Adelta-nociceptors recorded from UVB-inflamed (n=19) significantly diminished, by 50%, compared those naive (n=13). The heat-sensitive C-nociceptors unchanged while their heat increased, 75%, (n=26) (n=12). Heat-insensitive C-nociceptors, however, demonstrated enhanced (by 60%) stimulation (n=21) Notably alteration Adelta- heat-insensitive particular stronger stimuli. Spontaneous activity not this UVB. We conclude may be explained net shift nociceptor properties.