突触可塑性在肠道感染大鼠模型内脏高敏感形成中的意义

目的 研究旋毛虫感染SD大鼠后内脏敏感性变化和突触可塑性在内脏高敏感中的作用.方法 30只雄性SD大鼠均分为正常对照组、急性感染组(旋毛虫感染2周)和慢性感染组(旋毛虫感染8周).用不同结直肠压力20、40、60和80 mmHg(1 mmHg=0.133 kPa)]扩张10 S内诱发的腹壁肌电活动形成的曲线下面积(AUC)评估内脏敏感性.观察感染后不同时期结肠组织病理学变化.采用透射电镜观察结肠突触超微结构,RT-PCR和Western印迹法检测回盲部、近端结肠和远端结肠突触素和突触后致密物质(PSD)-95 mRNA和蛋白质水平的表达.结果 ①在40和60 mmHg的扩张压力下,慢性感染组AUC较正常对照组显著升高(P值分别=0.012和0.005);而急性感染组AUC较正常对照组显著降低(P值分别=0.018和0.012).②组织病理学评分结果 显示,急性感染组的炎症积分为23.45±4.10,较正常对照组(9.10±2.42,P=0.027)显著升高;而慢性感染组为13.95±7.96,与正常对照组差异无统计学意义(P=0.78).③急性感染组可见突触前膜线粒体嵴消失,线粒体肿胀或空泡化,与正常对照组相比囊泡数量显著减少,PSD长度显著减少.慢性感染组中,囊泡性质无明显变化,但数量较正常对照组大鼠明显增加,突触后膜电子致密物增厚,颜色加深,长度延长.三组间突触间隙无明显变化.④与正常对照组相比,慢性感染组大鼠回盲部、近端结肠和远端结肠突触素mRNA和蛋白的表达均显著升高(P值均＜0.05);而急性感染组突触素在mRNA和蛋白质水平的表达降低,但差异无统计学意义(P＞0.05).⑤与正常对照组相比,慢性感染组大鼠回盲部、近端结肠和远端结肠PSD-95mRNA和蛋白的表达均显著升高(P值均＜0.05);而急性感染组各部位PSD-95 mRNA和蛋白的表达显著降低(P值均＜0.05).结论 肠道感染大鼠模型内脏高敏感性的形成与突触可塑性有关.

The role of synaptic plasticity on rats with visceral hypersensitivity induced by transient intestinal infection

Objective To investigate the role of synaptic plasticity on the formation of visceral hypersensitivity induced by transient intestinal infection in rats. Methods Thirty male Sprague-Dawley rats were divided into normal control, acute infection and chronic infection groups with 10 each. The area under curve (AUC) of electromyography (EMG) in 10 s was used to evaluate the visceral sensitivity induced by different eolorectal distention (20,40,60 and 80 mmHg). Histological change of the colon was evaluated by H-E staining. Synaptic uhrastrueture such as synaptic cleft and synaptic vesicles was observed using transmission electron mieroseope. The mRNA and protein expressions of synaptophysin and postsynaptic density protein-95 (PSD-95) were examined by RT-PCR and Western blot, respectively. significantly higher than those of normal controls(P=0. 012, 0. 005, respectively ). In contrast, AUC of acute infection were significantly lower than those of normal controls ( P = 0. 018,0. 012, respectively ). Under the distention of 20 and 80 mmHg, no significant difference was observed among three groups (P= rats compared to normal controls(23.45±4.10 vs. 9.10±2.42, P=0. 027),but there was no statistical difference between chronic infection rats and normal controls (13. 95±7.96 vs. 9.15±2.42, P=0.78). increased. In acute infection rats, mitochondria cristae disappeared, synaptic vesicles and the length of controls, mRNA and protein of synaptophysin in ileocecum, proximal colon and distal colon were significantly increased in chronic infection rats (P＜0. 05 ), but decreased in acute infection rats with no significant difference. Compared with controls, no significant downregulation was noted in the expression protein expressions of PSD-95 were both increased in chronic infection rats (P＜0.05), and decreased in acute infection rats (P＜0.05). Conclusion Synaptic plasticity plays an important role in the formation of visceral hypersensitivity induced by transient intestinal infection in rats.