Chorda tympani (CT) nerve responses were recorded during simultaneous current and voltage clamping of the lingual receptive-field epithelium to examine the role of field potential in taste mixture suppression between sodium gluconate (NaG) and potassium gluconate (KG). 2. Under zero current-clamp conditions, CT responses to 100 mM NaG were suppressed by 63% when presented in mixture with 250 mM KG. At this concentration, KG alone elicited no measurable neural activity, but produced a large submucosal-positive field potential. 3. When CT responses to 100 mM NaG were obtained with voltage clamp at the zero-current clamp field potential of the NaG/KG mixture, they were suppressed by only 30% relative to NaG responses under zero-current clamp. Similarly, CT responses to the mixture of NaG and KG measured while voltage was clamped at the field potential of NaG alone were slightly elevated, but not to the magnitude of zero-current clamp responses to NaG. Therefore field potential-mediated suppression of CT responses to NaG accounts for only a part of the total mixture suppression between NaG and KG. 4. Analysis of the voltage dependence of CT responses to NaG indicated that the moderate field potential increase (8.9 mV) caused by the presence of KG in the mixture equates to a 43% increase in the apparent Km for NaG, from 110 to 157 mM. Use of this effective Km obviated the effect of field potential on CT responses to the NaG/KG mixture and permitted kinetic analysis of K+ blockade of Na+ responses. These analyses suggested that K ions block Na+ movement through apical Na+ channels in a voltage-independent manner with an apparent Ko of 405 mM. Importantly, direct inhibition of Na+ transduction by K+ can account for the part of mixture suppression not mediated by field potential. 5. These experiments reveal that mixture suppression between NaG and KG is derived from two distinct sources. Field potential, triggered largely by the limited mobility of both K+ and Na+ through taste bud tight junctions, globally modulates Na+ transduction. In addition, at the level of the apical Na+ channel, K ions directly block movement of depolarizing Na+ across taste receptor apical membranes.
摘要
在对舌感受野上皮进行电流钳制和电压钳制的同时，记录鼓索神经（CT）的反应，以研究场电位在葡萄糖酸钠（NaG）和葡萄糖酸钾（KG）之间味觉混合抑制中的作用。2. 在零电流钳制条件下，当与250 mM KG混合呈现时，CT对100 mM NaG的反应被抑制了63%。在此浓度下，单独的KG未引发可测量的神经活动，但产生了较大的黏膜下正场电位。3. 当在NaG/KG混合物的零电流钳制场电位下用电压钳获得CT对100 mM NaG的反应时，相对于零电流钳制下的NaG反应，它们仅被抑制了30%。同样，在电压钳制于单独NaG的场电位时测量的CT对NaG和KG混合物的反应略有升高，但未达到零电流钳制下对NaG反应的幅度。因此，场电位介导的对CT对NaG反应的抑制仅占NaG和KG之间总混合抑制的一部分。4. 对CT对NaG反应的电压依赖性分析表明，混合物中KG的存在导致的适度场电位增加（8.9 mV）相当于NaG的表观Km增加了43%，从110 mM增加到157 mM。使用这个有效的Km消除了场电位对CT对NaG/KG混合物反应的影响，并允许对K⁺对Na⁺反应的阻断进行动力学分析。这些分析表明，K离子以电压非依赖性方式阻断Na⁺通过顶端Na⁺通道的移动，表观Ko为405 mM。重要的是，K⁺对Na⁺转导的直接抑制可以解释场电位未介导的混合抑制部分。5. 这些实验表明，NaG和KG之间的混合抑制来自两个不同的来源。场电位主要由K⁺和Na⁺通过味蕾紧密连接的有限移动性触发，全局调节Na⁺转导。此外，在顶端Na⁺通道水平，K离子直接阻断去极化Na⁺跨味觉受体顶端膜的移动。
