Recordings of human polymodal single C-fiber afferents following mechanical and argon-laser heat stimulation of inflamed skin.
Activity in single C-fiber afferents, whose cutaneous receptive fields were on the dorsal side of the foot (n=10), were recorded in the peroneal nerve of healthy voluntary subjects. Characterization of the fibers with respect to thresholds and field areas were made before and after cutaneous inflammation, which was induced with mustard oil. To test the nociceptive heat modality, a high-intensity argon laser was used and single 200-ms light pulses were focused onto the skin. The mechanical properties were tested with von Frey-type filaments. In the uninflamed skin, heat and mechanical stimulation activated single C-fibers in matching skin areas. The areas were all within the receptive field borders defined by electrical cutaneous stimulation. The mustard-oil-induced cutaneous inflammation was subjectively reported by the subjects as being moderately painful. In six of the units, a spontaneous activity was induced in the sample of ten previously non-active units. Before the inflammation, the 200-ms argon-laser pulse evoked a highly reproducible pattern of spike-trains. Following inflammation, this pattern was reproducible, but appeared with a significantly reduced activation rate despite the same energy being delivered to the skin both before and after the inflammation. A reduction in slope of the stimulus-response relationship was also observed after inflammation. Following inflammation, changes occurred with expansion both of the mechanical- and heat-receptive fields. The expansion was delineated by the areas defined by electrical stimulation. Following inflammation, the threshold to heat was decreased, but that to mechanical stimuli was not. No relation was detected between the threshold change and the degree of receptive-field expansion. The subjective pain reported changed following inflammation with an increase in the perceived pain in relation to the recorded action potentials, which emphasizes the importance of either an increase in sensitivity in the central nervous system or an increase in peripheral spatial summation after inflammation.
Institute of Clinical Neuroscience, Department of Psychiatry and Neurochemistry, Sahlgrenska University Hospital/Mölndal, Sweden. bengt.olausson@ms.se
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Olausson
D000328:Adult; D000344:Afferent Pathways / Q000502:physiology; D001128:Argon; D003872:Dermatitis / Q000503:physiopathology*; D004558:Electric Stimulation; D006358:Hot Temperature; D006801:Humans; D007834:Lasers / Q000009:adverse effects*; D009412:Nerve Fibers / Q000502:physiology*; D009431:Neural Conduction / Q000502:physiology; D009474:Neurons / Q000502:physiology; D017288:Pain Threshold / Q000502:physiology; D011601:Psychophysics; D012867:Skin / Q000294:innervation; D013314:Stress, Mechanical
D001128:Argon