There is good evidence indicating that ion-transport pathways in the apical regions of lingual epithelial cells, including taste bud cells, may play a role in salt taste reception. In this article, we present evidence that, in the case of the dog, there also exists a sugar- activated ion-transport pathway that is linked to sugar taste transduction. Evidence was drawn from two parallel lines of experiments: (a) ion-transport studies on the isolated canine lingual epithelium, and (b) recordings from the canine chorda tympani. The results in vitro showed that both mono- and disaccharides in the mucosal bath stimulate a dose-dependent increase in the short-circuit current over the concentration range coincident with mammalian sugar taste responses. Transepithelial current evoked by glucose, fructose, or sucrose in either 30 mM NaCl or in Krebs-Henseleit buffer (K-H) was partially blocked by amiloride. Among current carriers activated by saccharides, the current response was greater with Na than with K. Ion flux measurements in K-H during stimulation with 3-O-methylglucose showed that the sugar-evoked current was due to an increase in the Na influx. Ouabain or amiloride reduced the sugar-evoked Na influx without effect on sugar transport as measured with tritiated 3-O-methylglucose. Amiloride inhibited the canine chorda tympani response to 0.5 M NaCl by 70-80% and the response to 0.5 M KCl by approximately 40%. This agreed with the percent inhibition by amiloride of the short-circuit current supported in vitro by NaCl and KCl. Amiloride also partially inhibited the chorda tympani responses to sucrose and to fructose. The results indicate that in the dog: (a) the ion transporter subserving Na taste also subserves part of the response to K, and (b) a sugar-activated, Na- preferring ion-transport system is one mechanism mediating sugar taste transduction. Results in the literature indicate a similar sweet taste mechanism for humans.
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机译：有充分的证据表明，包括味蕾细胞在内的舌上皮细胞的顶端区域中的离子运输途径可能在盐味的接收中起作用。在本文中，我们提供证据表明，在狗的情况下，还存在与糖味传导相关的糖活化离子转运途径。证据来自两条平行的实验线：（a）对离体犬舌上皮细胞的离子迁移研究，以及（b）犬霍乱鼓膜的录音。体外结果表明，在与哺乳动物糖味反应相一致的浓度范围内，粘膜浴中的单糖和二糖均刺激了短路电流的剂量依赖性增加。葡萄糖，果糖或蔗糖在30 mM NaCl或Krebs-Henseleit缓冲液（K-H）中引起的跨上皮电流被阿米洛利部分阻断。在被糖激活的电流载体中，Na的电流响应大于钾的电流响应。在3-O-甲基葡萄糖刺激过程中，K-H中的离子通量测量表明，糖诱发的电流是由于Na流入量的增加所致。用tri化的3-O-甲基葡萄糖测量，瓦巴因或阿米洛利减少了糖引起的钠流入，而对糖的转运没有影响。阿米洛利抑制对70 M-0.5 M NaCl的犬霍乱鼓膜的反应和对约40％的对0.5 M KCl的反应。这与阿米洛利对NaCl和KCl体外支持的短路电流的抑制百分数一致。阿米洛利也部分抑制了鼓膜对蔗糖和果糖的反应。结果表明，在狗中：（a）保留Na味的离子转运蛋白也保留了对K的部分响应，并且（b）糖激活的Na偏爱的离子转运系统是介导糖味传导的一种机制。文献中的结果表明了人类相似的甜味机制。
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