| Clinically, tissue injury can not only result in spontaneous pain and hyperalgesia in the injured site, but also, sometimes spontaneous pain and hyperalgesia in the mirror-image site. It is long found that tissue and nerve injury in one side of body can lead to pain in the mirror-image site, which is named as the mirror-image pain. To date, the mechanism underlying mirror-image pain is not clear. Recently, our results show that subcutaneous (s.c.) injection of bee venom into hindpaw of one side in rats can not only produce a persistent spontaneous nociception, primary heat and mechanical hyperalgesia and secondary heat hyperalgesia in the injected side, but also mirror-image heat hyperalgesia. The mirror-image hyperalgesia provides a good model to investigate the peripheral and central mechanism of clinical mirror-image pain. During studying for Master degree, it has been found that s.c. injection of bee venom can produce mirror-image heat hyperalgesia, which is spatially symmetric and temporally parallel to ipsilateral heat hyperalgesia (Chen and Chen 2000), and that the mirror-image heat hyperalgesia results from the central sensitization (Chen et al., 2000). Based on our previous results, the present study further investigates several questions as follows:a) Is central sensitization-maintained mirror-image heat hyperalgesia triggered byongoing activities from the peripheral injury site? Is the central sensitization determined by a time window of central summation of ongoing primary afferent input from a peripheral injury site?b) What peripheral primary afferent component is involved in the development of the experimental mirror-image heat hyperalgesia?c) Does the activation of RMM-spinal dorsal horn facilitatory system have effect on the development of the experimental mirror-image heat hyperalgesia?d) What roles do NMDA and non-NMDA receptors in the spinal cord play in the development of the experimental mirror-image heat hyperalgesia?The results:1. The experimental mirror-image heat hyperalgesia maintained by central sensitization is determined by a time window of central summation of ongoing primary afferent input from a peripheral injury site.Our previous study has demonstrated that central sensitization is responsible for bee venom-induced mirror-image heat hyperalgesia. The present study was designed to investigate whether central sensitization is determined by a time window of central summation of ongoing primary afferent input from a peripheral injury site. The results showed that after a dose of 0.2 mg BV, axotomy at 5 min completely prevented mirror-image heat hyperalgesia but was without effect at 10 min, whereas after a dose of 0.1 mg BV, axotomy at 10 min was able to prevent the mirror-image heat hyperalgesia but remained without effect at 20 min. These findings suggest an important role of the amount of ipsilateral ongoing primary afferent in establishing the mirror-image heat hyperalgesia.2. Involvement of capsaicin-sensitive primary afferent fibers in the experimental mirror-image heat hyperalgesiaTo further investigate what neural component in the periphery is involved in the bee venom-induced mirror-image heat hyperalgesia, we destroyed the capsaicin-sensitive primary afferent (CSPA) fibers by applying capsaicin, the main pungent ingredient of hot chili peppers, topically onto the sciatic and the saphenous nerves of rats under pentobarbital anesthesia. As a control, vehicle (Tween80:ethanol:Saline=l :1:8) was topically applied onto both the sciatic and the saphenous nerves or capsaicin onto the local muscle. The results showed that the destruction of capsaicin-sensitive primary afferents produced a significant suppression of the bee venom-induced persistent spontaneous flinches and a complete blockage of the mirror-image heat hyperalgesia, when compared with control treatment. These results suggest that the peripheral CSPA fibers are involved in the bee venom -induced persistent spontaneous nociception, and the mirr...
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