Transduction mechanism of four basic taste stimuli into electric signals of taste cell

1. 本项目旨在阐明味觉细胞在四种味觉刺激下产生受体电位的机制。利用原位蛙舌，将一个3 M充满氯化钾的微电极插入到真菌状乳头的单个味觉细胞中，记录细胞内受体电位。以0.5 M NaCl、1 mM HCl、10 mM奎宁-HCl （Q-HCl）和1 M半乳糖作为4种基本味觉刺激。通过去除舌表面液体中的一价和二价阳离子以及味觉细胞周围的间质液中的<Na^+>， NaCl的受体电位大大降低。因此，nacl诱导的受体电位是由离子电流流过受体膜的阳离子选择通道和基底膜的<Na^+>通道产生的。HCl受体电位不受间质离子的影响，但通过去除浅表液体中的<Ca^(2+)>和<Na^+>并加入速尿可大大抑制HCl受体电位。即使在舌头适应了水之后，也会产生较大的酸性反应。因此，盐酸诱导的反应大部分由受体膜的<Ca^(2+)>通道产生，其余部分由相边界电位产生。通过降低浅表液中的<Cl^->， Q-HCl受体电位显著升高，通过去除<Na^+>和<Ca^(2+)>并在间质液中加入速尿，Q-HCl受体电位降低。因此，大部分Q-HCl响应是由<Na^+> / <Cl^->共转运积累的<Cl^->释放产生的。在间质液中去除<Cl^->和加入DCCD可大大降低半乳糖受体电位，并通过降低表面液的pH值而增加。因此，我们认为半乳糖反应是由<OH^->的释放产生的，这与<Cl^->依赖的<H^+>泵有关。

1. The purpose of this project is to clarify the mechanisms underlying the generation of receptor potential of the taste cell in response to the four taste stimuli.2. The in situ frog tongues were used and intracellular receptor potentials were recorded from single taste cells of the fungiform papillae by inserting a 3 M KCl-filled microelectrode into the cell. As the four basic taste stimuli, 0.5 M NaCl, 1 mM HCl, 10 mM quinine-HCl (Q-HCl) and 1 M garactose were used.3. The receptor potential for NaCl was greatly reduced by removing mono- and divalent cations from the superficial fluid over the tongue and <Na^+> from the interstitial fluid surrounding taste cells. Therefore it is concluded that the NaCl-induced receptor potential is generated by ionic currents flowing cation-selective channel of the receptor membrane and <Na^+> channel of the basolateral membrane.4. The receptor potential for HCl was not affected by interstitial ions, but was greatly depressed by removing <Ca^(2+)> and <Na^+> in the superficial fluid and by adding furosemide to it. Even after adaptation of the tongue to water, large acid response was evoked. Therefore, the large portion of the HCl-induced response is generated by <Ca^(2+)> channel of the receptor membrane but the remaining portion is generated by the phase boundary potential.5. The receptor potential for Q-HCl was greatly increased by reducing <Cl^-> in the superficial fluid and was reduced by removing <Na^+> and <Ca^(2+)> and adding furosemide in the interstitial fluid. Therefore, the most of the Q-HCl response is generated by a release of <Cl^-> accumulated by a <Na^+> / <Cl^-> cotransport.6. The receptor potential for galactose was greatly reduced by removing <Cl^-> and adding DCCD in the interstitial fluid and increased by reducing a pH of superficial fluid. Thus it is suggested that the galactose response is generated by a release of <OH^-> which is related to <Cl^-> -dependent <H^+> pump.