目的:研究多节段背根节慢性压迫(chronic compression of multiple dorsal root ganglia,CCD)大鼠机械触刺激诱发痛镜像痛的外周机制。方法:制作单侧L3-L5 CCD模型大鼠,并应用von Frey filaments检测双侧机械触刺激诱发痛行为,利用免疫组织化学方法检测该模型大鼠同侧及对侧DRG大中型和小型神经元中与痛觉信息传递相关的神经肽-降钙素基因相关肽(calcitonin gene-related peptide,CGRP)的表达情况。结果:CCD大鼠表现出明显双侧机械触刺激诱发痛行为;免疫组织化学结果显示,CCD模型大鼠同侧及对侧DRG大和中等大小神经元内,CGRP的表达与正常组大鼠DRG神经元比较有明显升高(P〈0.05),而同侧及对侧DRG小神经元,CGRP的表达与正常组大鼠DRG神经元比较无明显变化(P〉0.05)。结论:CCD模型大鼠双侧DRG内传递痛觉信息的神经肽CGRP表达升高,提示外周双侧DRG神经元内CGRP的可塑性变化可能参与多节段CCD模型大鼠机械触刺激诱发痛镜像痛的发生。
Objective: To study the possible peripheral mechanism of mirror-image mechanical allodynia in the chronic compression of multiple dorsal root ganglia(multiple CCD) in rats.Methods: On the basis of unilateral compression of L3-L5 CCD model in the rat,the behavior of mechanical tactile allodynia on both sides were examined with von Frey filaments,and the expression of calcitonin gene-related peptide(CGRP),one pain transmission-related neuropeptide,in large or medium and small DRG neurons were examined with immunohistochemical technology on both sides of the DRGs.Results: An obviously behavior of both ipsilateral and contralateral mechanical tactile allodynia could be observed in the multiple CCD model,and there was an obviously high expression of CGRP in both ipsilateral and contralateral large and medium DRG neurons of multiple CCD group compared to control group(P〈0.05),while there was no significant changes of that in small DRG neurons compared to control group(P〉0.05).Conclusion: The pain transmission neuropeptide-CGRP was significantly increased in bilateral DRG neurons of multiple CCD rats,it suggest that the change of the plasticity of bilateral peripheral DRG neurons could be involved in the occurrence of mirror-image mechanical allodynia in the multiple CCD rats.