Acetylcholine metabolism in the inflamed rat intestine
Acetylcholine metabolism in the inflamed rat intestine
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DOI：
10.1006/exnr.1998.6839
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发表时间：
1998-08-01
影响因子：
5.3
通讯作者：
Blennerhassett, MG
中科院分区：
文献类型：
--
作者：
Davis, KAM;Masella, J;Blennerhassett, MG
乙酰胆碱（Acetylcholine，ACh）是肠神经系统的主要神经递质。由于越来越多的证据表明，炎症改变神经调节肠道功能，我们研究了乙酰胆碱的合成和分解的平滑肌/肌间神经丛（SM/MP）制剂从空肠的大鼠在炎症引起的线虫寄生虫旋毛虫感染。总的和神经元特异性摄取乙酰胆碱前体[H-3]胆碱到SM/MP制剂增加了两倍以上的感染后第6天。此外，胆碱乙酰转移酶活性的放射化学测定显示第1天显著增加，第3天达到峰值，此后保持不变。尽管这些步骤的增强，在体外SM/MP制剂中[H-3]胆碱转化为[3 H]ACh的测量结果显示，到第6天，[H-3]胆碱转化为[3 H]ACh的测量结果减少了近四倍，这意味着在发炎的空肠中ACh的产生大幅减少。大鼠空肠乙酰胆碱酯酶检查显示肌壁组织化学染色强度降低，定量评价显示SM/MP制剂中乙酰胆碱酯酶活性显著降低（>50%）。这些结果表明，胆碱能神经支配的肠道可以进行快速和持久的变化，在炎症。乙酰胆碱合成途径中的主要步骤的上调不匹配乙酰胆碱产量的增加，这表明乙酰胆碱包装，储存和颗粒胞吐的缺陷也可能存在。(C)北京：科学出版社.
Acetylcholine (ACh) is a major neurotransmitter in the enteric nervous system. Since increasing evidence suggests that inflammation alters neural regulation of intestinal function, we examined the synthesis and breakdown of ACh in smooth muscle/myenteric plexus (SM/MP) preparations from the jejunum of the rat during inflammation caused by infection with the nematode parasite Trichinella spiralis. Both total and neuron-specific uptake of the ACh precursor [H-3]choline into SM/MP preparations was increased by over twofold on Day 6 postinfection. Further, a radiochemical assay of choline acetyltransferase activity showed significant increase by Day 1, with peak values reached by Day 3 and maintained without reversal thereafter. Despite the enhancement of these steps, measurement of the conversion of [H-3]choline into [3H]ACh in SM/MP preparations in vitro showed a nearly fourfold decrease by Day 6, implying a large decrease in ACh production in the inflamed jejunum. Examination of acetylcholinesterase in the rat jejunum showed decreased histochemical staining intensity in the muscle wall, and quantitative evaluation showed significantly decreased (>50%) acetylcholinesterase activity in SM/MP preparations. These results show that cholinergic innervation of the intestine can undergo rapid and long-lasting alterations during inflammation. Upregulation of major steps in the synthetic pathway for ACh was not matched by increased ACh production, suggesting that defects in ACh packaging, storage, and granule exocytosis may also be present. (C) 1998 Academic Press.