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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >M3 muscarinic receptor-deficient mice retain bethanechol-mediated intestinal ion transport and are more sensitive to colitis.
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M3 muscarinic receptor-deficient mice retain bethanechol-mediated intestinal ion transport and are more sensitive to colitis.

机译：M3毒蕈碱受体缺陷型小鼠保留了苯乙二酚介导的肠道离子运输，对结肠炎更敏感。

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摘要

Acetylcholine (ACh) is an important regulator of intestinal epithelial ion transport via muscarinic or nicotinic ACh receptors. Previous studies emphasize the role of the M3 muscarinic receptor subtype in mediating the effects of cholinergic agonists on intestinal ion transport. With the prevalence of mouse models to study intestinal (patho)physiology, it is crucial that ion transport be understood in this species. Using M3 receptor-deficient (KO) mice and wild-type (WT) mice, we examined M3 receptor contributions to ion transport as well as its role in colitis induced by dextran sodium sulphate (DSS). In the Ussing chambers, ileal and colonic tissue from M3 KO and WT mice displayed similar baseline ion transport properties. Short-circuit current (ISC) responses to the muscarinic receptor agonist bethanechol were slightly decreased in ileal tissue from M3 KO mice compared with tissue from WT mice, whereas responses were not significantly different in colonic tissue. ISC responses to bethanechol were partially inhibited by pirenzepine in WT ileum, but not tetrodotoxin, suggesting involvement of a non-neuronal M1 muscarinic receptor. In the ileum, the M3 receptor may inhibit neuronally evoked ion transport, as indicated by the increased ISC responses to electrical stimulation in tissue from M3 KO mice. Furthermore, whereas all DSS-treated mice developed colitis, M3 KO mice displayed more rapid mass loss and more severe disease than DSS-treated WT mice, even following a reduction in the amount and time of DSS treatment. Thus, M3 receptor-KO mice are compensated in their ability to evoke muscarinic receptor-driven ion transport responses, but are more sensitive to DSS. This work highlights the need to dissect muscarinic receptor-mediated events in the mouse, as mice become increasingly valuable in enteric disease models.
机译：乙酰胆碱（ACh）是通过毒蕈碱或烟碱型ACh受体转运肠上皮离子的重要调节剂。先前的研究强调了M3毒蕈碱受体亚型在介导胆碱能激动剂对肠道离子运输的影响中的作用。随着研究肠道（病理）生理的小鼠模型的普及，了解该物种的离子转运至关重要。我们使用M3受体缺陷（KO）小鼠和野生型（WT）小鼠，我们检查了M3受体对离子转运的贡献以及其在右旋糖酐硫酸钠（DSS）诱导的结肠炎中的作用。在Ussing室中，来自M3 KO和WT小鼠的回肠和结肠组织显示出相似的基线离子传输特性。与WT小鼠相比，M3 KO小鼠回肠组织对毒蕈碱受体激动剂安息香的短路电流（ISC）响应略有降低，而结肠组织的响应无明显差异。哌仑西平在WT回肠中对Bethylchol的ISC反应受到部分抑制，但河豚毒素则无抑制作用，这表明非神经元M1毒蕈碱受体参与其中。在回肠中，M3受体可能抑制神经元诱发的离子转运，如M3 KO小鼠对组织中电刺激的ISC反应增强所表明的。此外，尽管所有DSS治疗的小鼠都患有结肠炎，但即使DSS治疗的数量和时间减少，M3 KO小鼠也比DSS治疗的WT小鼠表现出更快的质量损失和更严重的疾病。因此，M3受体-KO小鼠引起毒蕈碱受体驱动的离子转运反应的能力得到了补偿，但对DSS更为敏感。这项工作突显了在小鼠中剖析毒蕈碱受体介导的事件的必要性，因为小鼠在肠道疾病模型中的价值越来越高。

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