A modified animal model of mirror-image pain in unilateral compressions of multiple DRGs of the rat

Abstract

Mirror-image pain is the pain phenomenon being recognized at contralateral symmetrical area from original injured region. The pain sensation from the contralateral side is qualitatively similar to the original pain, but less prominent. Bilateral effects of unilateral injury are very common phenomena in chronic pain patients and experimental animal pain models. However, our knowledge of the mechanisms underlying such spreading of pain is currently very limited due to reliable animal model of chronic mirror-image pain. Targeted at multiple level rediculopathies in common, the compression of multiple DRGs of lumbar 3, 4 and 5 was established in the rat with the modification of CCD model. Pain behavior of mechanical allodynia and its possible mechanism were further investigated with immunochemical methods in the present study. It was showed that both ipsilateral and contralateral mechanical thresholds were significantly decreased in a unilateral compression of multilple CCD model. Furthermore, both ipsilateral and contralateral response scores to acetone were obviously increased after the chronic compression of multiple DRGs. The expression of activating transcription factor 3 (ATF3, a marker of nerve injury) and calcitonin gene-related peptide (CGRP) was significantly increased in ipsilateral and contralateral DRGs in multiple CCD rats, and the increased change mainly occurred in large- and medium-sized DRG neurons or large- and medium-sized, and small DRG neurons, respectively. In summary, a unilateral compression of multilple DRG model exhibited an obvious mirror-image pain stably. Contralateral neuropathology in the DRG may contribute to mirror-image mechanical and cold allodynia, and thermal hyperalgesia in unilateral compressions of multiple DRGs of the rat. This more reliably mirror-image pain animal model would be useful to elucidate the mechanisms of mirror-image pain of either allodynia or hyperalgesia in humans. Acknowledgement This work was supported by grants from the National Natural Science Foundation of China (No. 30870830 to Dr. H.X.).