Yoshii K, Yotsui C
Dept. of Biochemical Engineering and Science, Kyushu Institute of Technology, Fukuoka, Japan.
Brain Res. 1997 May 23;757(2):202-8. doi: 10.1016/s0006-8993(97)00219-9.
We investigated the effects of intracellular pH values (pHi) on taste nerve responses of clawed toads and eels. (1) CO2, NH3 or trimethylamine reversibly suppressed the taste nerve responses of clawed toads to various amino acids, CaCl2 and caffeine. IC50 values of the suppression of the responses to 0.1 mM L-proline were as follows: approximately 10 mM for CO2, approximately 0.3 mM for NH3, approximately 0.2 mM for trimethylamine. (2) Cross-adaptation experiments showed that L-proline, caffeine and CaCl2 stimulated different receptor sites from each other, indicating the suppressive effect was non-specific. (3) Although CO2, NH3 or trimethylamine yielded the charged molecules, HCO3-, CO3(2-), NH4+ or trimethylammonium on hydration, none of these charged species suppressed taste responses. (4) NH3 increased the threshold concentration of L-proline by e-fold per 0.37 mM NH3 and decreased the maximum response to L-proline with increasing NH3 concentration. (5) The taste nerve responses of eels to 0.1 mM L-arginine, a potent stimulus on eel taste receptors, were similarly suppressed by NH3 with an IC50 value of approximately 0.3 mM. (6) These results indicated that these uncharged species changed pHi, which suppressed the taste responses. CO2-induced acidosis and NH3- or trimethylamine-induced alkalosis are likely to inhibit activities of ion channels or enzymes involved in taste transduction mechanisms.
我们研究了细胞内pH值(pHi)对爪蟾和鳗鱼味觉神经反应的影响。(1)二氧化碳、氨或三甲胺可逆地抑制爪蟾对各种氨基酸、氯化钙和咖啡因的味觉神经反应。对0.1 mM L-脯氨酸反应抑制的半数抑制浓度(IC50)值如下:二氧化碳约为10 mM,氨约为0.3 mM,三甲胺约为0.2 mM。(2)交叉适应实验表明,L-脯氨酸、咖啡因和氯化钙刺激彼此不同的受体位点,表明抑制作用是非特异性的。(3)尽管二氧化碳、氨或三甲胺在水化时产生带电分子,即碳酸氢根离子、碳酸根离子、铵离子或三甲铵离子,但这些带电物质均未抑制味觉反应。(4)氨使L-脯氨酸的阈值浓度每增加0.37 mM增加e倍,并随着氨浓度的增加降低对L-脯氨酸的最大反应。(5)鳗鱼对0.1 mM L-精氨酸(对鳗鱼味觉受体的有效刺激物)的味觉神经反应同样被氨抑制,IC50值约为0.3 mM。(6)这些结果表明,这些不带电物质改变了pHi,从而抑制了味觉反应。二氧化碳诱导的酸中毒以及氨或三甲胺诱导的碱中毒可能会抑制参与味觉转导机制的离子通道或酶的活性。