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1 Neuropathic Pain Unit, Hospital General de Catalunya, Barcelona, Spain
2 Departamento de Ciencias Neurologicas, Universidad de Chile, Santiago, Chile
3 Sobell Department, Institute of Neurology, University College London, Queen Square, London, United Kingdom
4 Oregon Nerve Center, Good Samaritan Hospital and Medical Center, Oregon Health Sciences University, Portland, USA
* To whom correspondence should be addressed. E-mail: jserrac{at}meditex.es.
Peripheral nociceptor sensitization is accepted as an important mechanism of cutaneous primary hyperalgesia, but secondary hyperalgesia has been attributed to central mechanisms, since evidence for sensitization of primary afferents has been lacking. In this study, microneurography was used to test for changes in sensitivity of C nociceptors in the area of secondary hyperalgesia caused by intradermal injection of capsaicin in humans. Multiple C units were recruited by electrical stimulation of the skin at 0.25 Hz, and were identified as discrete series of dots in raster plots of spike latencies. Nociceptors slowed progressively during repetitive stimulation at 2 Hz for 3 minutes. According to their response to mechanical stimulation, nociceptors could be classified as either mechano-sensitive (CM) or mechano-insensitive (CMi). These two nociceptor subtypes had different axonal properties: CMi units slowed by 2% or more when stimulated at 0.25 Hz after a 3-minute pause, whereas CM units slowed by less than 1%. This stimulation protocol was used before capsaicin injection to identify nociceptor subtype without repeated probing, thus avoiding possible mechanical sensitization. Capsaicin, injected 10 to 50 mm away from the site of electrical stimulation, had no effect on any of 29 CM units, but induced bursts of activity in 11 out of 15 CMi units, after delays ranging from 0.5 to 18 minutes. The capsaicin injections also sensitized a majority of the CMi units, so that 11 out of 17 developed immediate or delayed responsiveness to mechanical stimuli. This sensitization may contribute a peripheral C fiber component to secondary hyperalgesia.
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