Yang Chang-Qing, Duan Li-Ping, Qiao Pei-Tang, Zhao Li, Guo Li-Li
Chang-Qing Yang, Pei-Tang Qiao, Li Zhao, Li-Li Guo, Department of Gastroenterology, Peace Hospital, Changzhi Medical College, Changzhi 046000, Shanxi Province, China.
World J Gastroenterol. 2015 Mar 14;21(10):2959-66. doi: 10.3748/wjg.v21.i10.2959.
To investigate the activity of vesicular glutamate transporter-3 (VGLUT3) in a visceral hyperalgesia rat model of irritable bowel syndrome, and the role of mast cells (MCs).
Transient intestinal infection was induced by oral administration of Trichinella spiralis larvae in rats. On the 100(th) day post-infection (PI), the rats were divided into an acute cold restraint stress (ACRS) group and a non-stressed group. Age-matched untreated rats served as controls. The abdominal withdrawal reflex was used to measure the visceromotor response to colorectal distension (CRD). The expression levels of VGLUT3 in peripheral and central neurons were analyzed by immunofluorescence and western blotting.
VGLUT3 expression in the L6S1 dorsal root ganglion cells was significantly higher in the PI group than in the control group (0.32 ± 0.009 vs 0.22 ± 0.008, P < 0.01), and there was no significant difference in the expression of VGLUT3 between MC-deficient rats and their normal wild-type littermates. Immunofluorescence showed that the expression levels of VGLUT3 in PI + ACRS rats were enhanced in the prefrontal cortex of the brain compared with the control group.
VGLUT3 is involved in the pathogenesis of visceral hyperalgesia. Coexpression of c-fos, 5-hydroxytryptamine and VGLUT3 after CRD was observed in associated neuronal pathways. Increased VGLUT3 induced by transient intestinal infection was found in peripheral nerves, and was independent of MCs. Moreover, the expression of VGLUT3 was enhanced in the prefrontal cortex in rats with induced infection and stress.
研究肠易激综合征内脏痛觉过敏大鼠模型中囊泡谷氨酸转运体3（VGLUT3）的活性以及肥大细胞（MCs）的作用。
通过给大鼠口服旋毛虫幼虫诱导短暂性肠道感染。在感染后第100天，将大鼠分为急性冷束缚应激（ACRS）组和非应激组。年龄匹配的未处理大鼠作为对照。采用腹部退缩反射来测量对结直肠扩张（CRD）的内脏运动反应。通过免疫荧光和蛋白质印迹法分析外周和中枢神经元中VGLUT3的表达水平。
感染组L6S1背根神经节细胞中VGLUT3的表达明显高于对照组（0.32±0.009对0.22±0.008，P<0.01），MC缺陷大鼠与其正常野生型同窝仔鼠之间VGLUT3的表达无显著差异。免疫荧光显示，与对照组相比，PI + ACRS大鼠脑前额叶皮质中VGLUT3的表达水平增强。
VGLUT3参与内脏痛觉过敏的发病机制。在相关神经通路中观察到CRD后c-fos、5-羟色胺和VGLUT3的共表达。发现短暂性肠道感染诱导的VGLUT3在外周神经中增加，且与MCs无关。此外，在诱导感染和应激的大鼠中，前额叶皮质中VGLUT3的表达增强。
