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首页> 外文期刊>Journal of neuroinflammation >Up-regulation of brain-derived neurotrophic factor in primary afferent pathway regulates colon-to-bladder cross-sensitization in rat
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Up-regulation of brain-derived neurotrophic factor in primary afferent pathway regulates colon-to-bladder cross-sensitization in rat

机译：初级传入途径中脑源性神经营养因子的上调调节大鼠结肠至膀胱的交叉敏化

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Background In humans, inflammation of either the urinary bladder or the distal colon often results in sensory cross-sensitization between these organs. Limited information is known about the mechanisms underlying this clinical syndrome. Studies with animal models have demonstrated that activation of primary afferent pathways may have a role in mediating viscero-visceral cross-organ sensitization. Methods Colonic inflammation was induced by a single dose of tri-nitrobenzene sulfonic acid (TNBS) instilled intracolonically. The histology of the colon and the urinary bladder was examined by hematoxylin and eosin (H&E) stain. The protein expression of transient receptor potential (TRP) ion channel of the vanilloid type 1 (TRPV1) and brain-derived neurotrophic factor (BDNF) were examined by immunohistochemistry and/or western blot. The inter-micturition intervals and the quantity of urine voided were obtained from analysis of cystometrograms. Results At 3 days post TNBS treatment, the protein level of TRPV1 was increased by 2-fold (p < 0.05) in the inflamed distal colon when examined with western blot. TRPV1 was mainly expressed in the axonal terminals in submucosal area of the distal colon, and was co-localized with the neural marker PGP9.5. In sensory neurons in the dorsal root ganglia (DRG), BDNF expression was augmented by colonic inflammation examined in the L1 DRG, and was expressed in TRPV1 positive neurons. The elevated level of BDNF in L1 DRG by colonic inflammation was blunted by prolonged pre-treatment of the animals with the neurotoxin resiniferatoxin (RTX). Colonic inflammation did not alter either the morphology of the urinary bladder or the expression level of TRPV1 in this viscus. However, colonic inflammation decreased the inter-micturition intervals and decreased the quantities of urine voided. The increased bladder activity by colonic inflammation was attenuated by prolonged intraluminal treatment with RTX or treatment with intrathecal BDNF neutralizing antibody. Conclusion Acute colonic inflammation increases bladder activity without affecting bladder morphology. Primary afferent-mediated BDNF up-regulation in the sensory neurons regulates, at least in part, the bladder activity during colonic inflammation.
机译：背景技术在人类中，膀胱或远端结肠的炎症通常会导致这些器官之间的感觉交叉敏化。关于此临床综合征潜在机制的信息知之甚少。动物模型研究表明，主要传入途径的激活可能在介导内脏内脏跨器官致敏中起作用。方法通过结肠内滴注单剂量三硝基苯磺酸（TNBS）诱导结肠炎症。用苏木精和曙红（H＆E）染色检查结肠和膀胱的组织学。通过免疫组织化学和/或蛋白质印迹检查了类香草素1型（TRPV1）和脑源性神经营养因子（BDNF）的瞬时受体电位（TRP）离子通道的蛋白表达。排尿间隔时间和排尿量是通过对膀胱测压图进行分析得出的。结果TNBS治疗后3天，用Western blot检测发炎的远端结肠中TRPV1的蛋白水平增加了2倍（p <0.05）。 TRPV1主要表达在远端结肠粘膜下区域的轴突末端，并与神经标记物PGP9.5共定位。在背根神经节（DRG）的感觉神经元中，通过L1 DRG中检查的结肠炎症增强了BDNF的表达，并在TRPV1阳性神经元中表达了BDNF。通过长时间用神经毒素树脂毒素（RTX）对动物进行预处理，可以减轻结肠炎引起的L1 DRG中BDNF的升高水平。结肠炎症既不改变膀胱的形态，也不改变该内脏中TRPV1的表达水平。但是，结肠发炎缩短了排尿间隔，并减少了排尿量。延长的腔内用RTX或鞘内BDNF中和抗体治疗可减轻结肠炎症引起的膀胱活动增加。结论急性结肠炎可增加膀胱活动性，而不影响膀胱形态。感觉神经元中的初级传入介导的BDNF上调至少部分调节结肠炎症期间的膀胱活动。

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