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PLCβ2-Independent Behavioral Avoidance of Prototypical Bitter-Tasting Ligands

机译:原型苦味配体的PLCβ2独立行为避免

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摘要

Using a brief-access taste assay, we show in the present report that although phospholipase C β2 knockout (PLCβ2 KO) mice are unresponsive to low- and midrange concentrations of quinine and denatonium, they do significantly avoid licking higher concentrations of these aversive compounds. PLCβ2 KO mice displayed no concentration-dependent licking of the prototypical sweetener sucrose but were similar to wild-type mice in their responses to citric acid and NaCl, notwithstanding some interesting exceptions. Although these findings confirm an essential role for PLCβ2 in taste responsiveness to sucrose and to low- to midrange concentrations of quinine and denatonium in mice as previously reported, they importantly suggest that higher concentrations of the latter two compounds, which are bitter to humans, can engage a PLCβ2-independent taste transduction pathway.
机译:使用简短的味觉分析,我们在本报告中显示,尽管磷脂酶Cβ2敲除(PLCβ2KO)小鼠对低和中等浓度的奎宁和地那铵没有反应,但它们确实避免了舔食这些厌恶化合物的更高浓度。尽管有一些有趣的例外,PLCβ2KO小鼠对原型甜味剂蔗糖没有表现出浓度依赖性的舔食,但它们对柠檬酸和NaCl的反应与野生型小鼠相似。尽管这些发现证实了PLCβ2在小鼠中对蔗糖以及对中低浓度的奎宁和地那铵的味觉响应中的重要作用,但重要的是,它们重要地表明,较高浓度的后两种化合物(对人类而言是苦的)可以参与独立于PLCβ2的味觉转导途径。

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