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首页> 外文期刊>The European Journal of Neuroscience >Increased expression of TRPV1 receptor in dorsal root ganglia by acid insult of the rat gastric mucosa.
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Increased expression of TRPV1 receptor in dorsal root ganglia by acid insult of the rat gastric mucosa.

机译：大鼠胃粘膜的酸侵害增加了背根神经节中TRPV1受体的表达。

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Abstract It is still unknown which receptors of peripheral sensory pathways encode and integrate an acid-induced nociceptive event in the gastric mucosa. The transient receptor potential vanilloid receptor 1 (TRPV1) and the acid-sensing ion channel 3 (ASIC3) are two nociception-related receptors. Here we investigated (i) to what extent these receptors are distributed in stomach-innervating neurons of dorsal root and nodose ganglia, using immunohistochemistry and retrograde tracing, and (ii) whether their expression is altered in response to a noxious acid challenge of the stomach. We also explored the presence of TRPV1 in the gastric enteric nervous system because of its possible expression by intrinsic sensory neurons. Most stomach-innervating neurons in nodose ganglia were immunoreactive for TRPV1 (80%) and ASIC3 (75%), these results being similar in the dorsal root ganglia (71 and 82%). RT-PCR and Western blotting were performed up to 6 h after oral application of 0.5 m HCl to conscious rats. TRPV1 protein was increased in dorsal root but not in nodose ganglia whereas TRPV1 and ASIC3 mRNAs remained unchanged. TRPV1 mRNA was detected in longitudinal muscle-myenteric plexus preparations of control stomachs and was not altered by the acid challenge. Combined vagotomy and ganglionectomy abolished expression of TRPV1, indicating that it may derive from an extrinsic source. In summary, noxious acid challenge of the stomach increased TRPV1 protein in spinal but not vagal or intrinsic sensory afferents. The TRPV1 receptor may be a key molecule in the transduction of acid-induced nociception of the gastric mucosa and a mediator of visceral hypersensitivity.
机译：摘要尚不清楚外周感觉途径的哪些受体编码和整合酸诱导的胃粘膜伤害性事件。瞬时受体电位类香草酸受体1（TRPV1）和酸敏感离子通道3（ASIC3）是两个与伤害感受有关的受体。在这里，我们使用免疫组织化学和逆行示踪方法研究了（i）这些受体在背根神经节和结节神经节的神经支配神经元中的分布程度，以及（ii）是否响应胃中的有害酸攻击而改变了其表达。我们还探讨了TRPV1在胃肠神经系统中的存在，因为它可能由内在的感觉神经元表达。结节神经节中大多数神经支配神经元对TRPV1（80％）和ASIC3（75％）具有免疫反应性，这些结果在背根神经节中相似（71和82％）。在对清醒的大鼠口服0.5 m HCl后长达6 h进行RT-PCR和蛋白质印迹。 TRPV1蛋白在背根中增加，但在结节神经节中没有增加，而TRPV1和ASIC3 mRNA则保持不变。在对照胃的纵向肌肉-肠系膜神经丛制剂中检测到TRPV1 mRNA，并且不受酸刺激的影响。联合迷走神经切断术和神经节切除术消除了TRPV1的表达，表明它可能源自外部来源。总之，胃中的有害酸刺激增加了脊髓中TRPV1蛋白的表达，但迷走神经或固有感觉传入蛋白却没有。 TRPV1受体可能是酸诱导胃粘膜伤害感受和内脏超敏性介导的关键分子。

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