Abstract
The spared nerve injury (SNI) model of neuropathic pain was first developed by Decosterd and Woolf in 2000 in Sprague Dawley rats to enhance reproducibility of injury and behavioral responses resulting from a partial nerve injury. Given the differences in methodology and inconsistent behavioral data published in the SNI model of neuropathic pain in mice, and given that interspecies behavioral comparisons using the same peripheral nerve injury are presently lacking, in this study we assessed the development of mechanical and cold allodynia for five weeks in C57BL/6 mice and Sprague Dawley rats that underwent SNI. In rats and mice, the tibial and peroneal branches were ligated then severed, leaving the sural branch intact. By controlling several factors in the surgical procedure and behavioral tests, we found that rats developed and maintained strong mechanical and robust cold allodynia immediately following the injury that was maintained for the duration of the experiment (five weeks). In comparison, mice developed mechanical allodynia to a lesser magnitude which peaked at 2 weeks, but did not develop cold allodynia. We found both temporal and qualitative differences in the development of allodynic behaviors between SNI-mice and SNI-rats. Parallel analysis of interspecies differences can be exploited to reveal novel molecular players leading to divergent pain behaviors.
Highlights
BackgroundPersistent post-operative pain (PPP) can be a consequence of nerve injury [1]
Though mechanical allodynia peaked at post-operative day (POD) 1 and was maintained until POD 35 in rats, it took approximately 2 weeks for mechanical allodynia to peak in mice (POD 14)
A multi-model approach is necessary to study the mechanisms of neuropathic pain, but it is usually reserved for examining differences in various peripheral nerve injury models within the same species [3] [7] [19], or for examining the same injury model in different strains of the same species [20] [21]
Summary
BackgroundPersistent post-operative pain (PPP) can be a consequence of nerve injury [1]. Animal models allow for a systematic and well-controlled environment whereby each of these variables can be independently or concomitantly examined and are useful for identifying potential therapeutic targets for neuropathic pain. Even though both mice and rats are routinely used in pre-clinical pain models, interspecies comparisons using the same, established nerve injury model are scarce. SNI is advantageous over other partial nerve injury models (partial sciatic nerve ligation, chronic constriction injury, and spinal nerve ligation) because the level of injury is reproducible It produces robust behavioral changes in rats, and affords the potential to study both injured and non-injured nerves and associated skin territories [3]. Reported inconsistencies within strain and within injury models become problematic
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