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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。
Aims: To investigate the peripheral mechanism of mechanical pain-stimulating pain in painful multi-segment dorsal root ganglia (CCD) rats. Methods: The unilateral L3-L5 CCD model rats were made. The von Frey filaments were used to detect the pain behavior induced by bilateral mechanical stimulation. The ipsilateral and contralateral DRG large and medium-sized and small neurons were detected by immunohistochemistry In the expression of neuropeptide calcitonin gene-related peptide (CGRP), which is related to the transmission of pain information. Results: The painful behaviors of CCD rats were obviously stimulated by bilateral mechanical stimulation. Immunohistochemistry showed that the expressions of CGRP in the large and medium DRG neurons in ipsilateral and contralateral DRG of CCD model rats were significantly higher than those in normal rats (P <0.05). The expression of CGRP and DRG neurons in the ipsilateral and contralateral DRG neurons were not significantly different from those in the normal group (P> 0.05). Conclusion: The expression of neuropeptide CGRP in bilateral DRG of rats with pain in CCD model rats is increased, suggesting that the plasticity of CGRP in peripheral DRG neurons may be involved in the painful pain-induced painful image of multi-segment CCD model rats occur.