Can the sensitization of nociceptors account for hyperalgesia after skin injury?
Psychophysical measurements of pain during heat stimulation of the skin were compared with electro-physiological recordings of heat-evoked discharge in C-fiber mechanoheat sensitive (CMH) nociceptors (C-polymodal nociceptors) in humans and in monkeys and A-fiber mechanoheat (AMH) nociceptors and low threshold thermoreceptors in monkeys before and after a mild heat injury of the skin. The only source of peripheral neural information that could be identified as contributing to the development of hyperalgesia (increased pain sensitivity) after the injury was the sensitization of CMH nociceptors, although the magnitude of sensitization could not fully account for the magnitude of hyperalgesia.
D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D002056:Burns / Q000503:physiopathology*; D005073:Evoked Potentials, Somatosensory; D000882:Haplorhini; D006801:Humans; D006930:Hyperalgesia / Q000503:physiopathology*; D006941:Hyperesthesia / Q000503:physiopathology*; D009619:Nociceptors / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000503:physiopathology; D011601:Psychophysics; D012684:Sensory Thresholds; D012867:Skin / Q000294:innervation*; D013116:Spinal Cord / Q000503:physiopathology; D009435:Synaptic Transmission; D013823:Thermoreceptors / Q000503:physiopathology; D013697:Thermosensing / Q000502:physiology