Effect of capsaicin treatment on nociceptors in rat glabrous skin one day after plantar incision.
Dilute capsaicin produces a differential effect on incision-related pain behaviors depending upon the test; it reduces heat hyperalgesia and guarding pain but not mechanical hyperalgesia. This suggests that common mechanisms for heat hyperalgesia and guarding pain occur, and distinct mechanisms exist for mechanical hyperalgesia. The purpose of the present study was to evaluate the effect of capsaicin treatment on the activity of cutaneous nociceptors sensitized by incision to understand the mechanisms for the selective action of dilute capsaicin on incisional pain. We compared the effect of 0.05% capsaicin vs. vehicle treatment on pain behaviors after incision and on the activity of nociceptors from these same rats using the in vitro glabrous skin-nerve preparation. Immunohistochemical expression of protein gene product 9.5 (PGP9.5), neurofilament 200, calcitonin gene related peptide (CGRP) and isolectin B4 (IB4) in skin was also evaluated 1 week after 0.05% capsaicin infiltration. Infiltration of 0.05% capsaicin decreased CGRP and IB4/PGP9.5-immunoreactivity of nociceptors in skin. The same dose of capsaicin that inhibited heat hyperalgesia and guarding behavior interfered with chemo- and heat sensitivity of C-fibers. Neither mechanical hyperalgesia nor mechanosensitivity of nociceptors was affected by capsaicin, suggesting that the concentration of capsaicin used in this study did not cause fiber degeneration. These results demonstrate that nociceptors desensitized by capsaicin contribute to heat hyperalgesia and guarding pain after plantar incision. These putative TRPV1-expressing C-fibers are sensitized to heat and acid after incision, and the transduction of heat and chemical stimuli after plantar incision is impaired by dilute capsaicin.
Kang
Sinyoung
S
Department of Anesthesia, University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA Department of Pharmacology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA Department of Anesthesia, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China Pain Research Program, New Jersey Neuroscience Institute at John F. Kennedy Medical Center, Edison, NJ 08820, USA.
Wu
Chaoran
C
Banik
Ratan K
RK
Brennan
Timothy J
TJ
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002211:Capsaicin / Q000494:pharmacology / Q000627:therapeutic use*; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000145:classification / Q000503:physiopathology; D037102:Lectins / Q000378:metabolism; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000378:metabolism; D009431:Neural Conduction / Q000502:physiology; D016900:Neurofilament Proteins / Q000378:metabolism; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000187:drug effects; D010149:Postoperative Pain / Q000188:drug therapy* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018689:Sensory System Agents / Q000627:therapeutic use*; D012867:Skin / Q000187:drug effects* / Q000294:innervation / Q000378:metabolism; D018709:Statistics, Nonparametric; D013268:Stimulation, Chemical; D043222:Ubiquitin Thiolesterase / Q000378:metabolism
D037102:Lectins; D016900:Neurofilament Proteins; D018689:Sensory System Agents; C051774:neurofilament protein H; C489034:UCHL1 protein, rat; D043222:Ubiquitin Thiolesterase; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin