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Ionic basis of receptor potential of frog taste cells induced by acid stimuli.

机译:酸刺激诱导青蛙味觉细胞受体电位的离子基础。

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摘要

1. The ionic mechanism underlying the receptor potential in frog taste cells induced by acid stimuli was studied with single microelectrodes by replacing superficial and interstitial fluids of the tongue with modified saline solutions. 2. The removal of Na+, Ca2+ and Cl- from the normal interstitial fluid did not affect the receptor potential induced by acid stimuli. Interstitial 100 mM-K+ saline did not affect the acid response. 3. The receptor potential was reduced greatly when Ca2+ was removed from the superficial saline, but was increased when the Ca2+ concentration was elevated. The removal of superficial Cl- did not affect the receptor potential. The receptor potential elicited by superficial Ca2+-free saline was partly due to Na+. Li+, K+, NH4+ or choline + substituted for Na+ in producing the receptor potential. The amiloride-sensitive Na+ channel on the receptor membrane did not contribute to the receptor potential. With pure water adaptation of the tongue surface, the mean magnitude of the acid response was 35% of the control. 4. The receptor potential was unaffected by superficial tetrodotoxin (TTX) but was blocked by superficial Ca2+ antagonists such as Co2+ and Cd2+. Sr2+ substituted for Ca2+ in generating the receptor potential. 5. The receptor potentials observed under various concentrations of superficial Ca2+ became smaller when Na+ was present in the superficial fluid, indicating a competition between Ca2+ and Na+. 6. It is concluded that a large portion of the receptor potential induced by acid stimuli is produced by cations passing through a tastant-gated Ca2+ channel on the taste receptor membrane. Both divalent (Ca2+, Sr2+) and monovalent (Na+, Li+, K+, NH4+, choline+) cations can pass through the Ca2+ channel. The other mechanism responsible for the remaining part of the receptor potential is discussed.
机译:1.用单个微电极研究了酸刺激在青蛙味觉细胞中由青蛙刺激的受体电位所依据的离子机制,该方法通过用改良盐溶液代替舌头的表层和组织液。 2.从正常的组织液中去除Na +,Ca2 +和Cl-不会影响酸刺激引起的受体电位。间质性100 mM-K +盐水不影响酸反应。 3.当从表面盐水中去除Ca2 +时,受体电位大大降低,但当Ca2 +浓度升高时,受体电位升高。表面Cl-的去除不影响受体电位。表面无Ca2 +的盐水引起的受体电位部分归因于Na +。 Li +,K +,NH4 +或胆碱+在产生受体电位时取代了Na +。受体膜上对阿米洛利敏感的Na +通道对受体电位没有贡献。通过舌头表面的纯净水适应,酸反应的平均幅度为对照的35%。 4.受体电位不受表面河豚毒素(TTX)的影响,但被表面Ca2 +拮抗剂(例如Co2 +和Cd2 +)阻断。 Sr2 +代替Ca2 +产生受体电势。 5.当表层流体中存在Na +时,在各种浓度的表层Ca2 +下观察到的受体电势变小,表明Ca2 +与Na +之间存在竞争。 6.结论是,由酸刺激诱导的大部分受体电位是由阳离子穿过味觉受体膜上的味觉控制的Ca2 +通道产生的。二价(Ca2 +,Sr2 +)和一价(Na +,Li +,K +,NH4 +,胆碱+)阳离子都可以通过Ca2 +通道。讨论了负责受体电位剩余部分的另一种机制。

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