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Differential Transdution Mechanisms Underlying NaCl- and KCl-induced Responses in mouse Taste Cells

机译:NaCl和KCl诱导的小鼠味觉细胞反应的差异传导机制

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The transduction mechanism of salt-induced responses of mouse taste cells was investigated using the patch clamp and the ocal stimul~ion techniques under quasi-natural conditions. Apically applied NaC! induced a voltage-independent current, Nhich was ~rtially suppressed by amiloride and Cd2+. In contrast, apically applied 0.5 M KC! induced an inwardly rectifying :urrent (KC!-rhduced lir). The KC!-induced lir was unaffected by amiloride. The lir was suppressed not only by external 8a2+ and :s+ , but also bya C!- channel blocker, niflumic acid. The Er of the KC!-induced response was independent of the apical ionic :oncentration, but rather was close to the equilibrium potential of C!- (Ea) at the basolateral membrane. The KC!-induced /ir jisplayed a fast run-down under the conditions of the conventional whole cell clamp method, but not under the perforated )atch conditions. Immunohistochemical localization of an inwardly rectifying C!- channel protein, C!C-2, was observed in taste )ud cells of the fungiform papillae. It is concluded that the transduction mechanism of NaC!-induced responses is completely jifferent from that of KC!-induced responses in mouse taste cells.
机译:在半自然条件下,使用膜片钳和ocal刺激技术研究了盐诱导的小鼠味觉细胞反应的转导机制。实际应用的NaC!感应电压无关的电流,Nhich在一定程度上被阿米洛利和Cd2 +抑制。相反,实际应用0.5 M KC!引起内向纠正:urrent(KC!-rhduced lir)。由KC!诱导的lir不受阿米洛利的影响。不仅通过外部的8a2 +和:s +抑制了lir,而且通过C!-通道阻滞剂尼氟酸也抑制了lir。 KC 1诱导的反应的Er与顶端离子的浓度无关,而是接近基底外侧膜上C 1-(Ea)的平衡电位。在常规的全细胞钳制方法条件下,但在穿孔捕获条件下,由KC!诱导的/ ir迅速发挥作用。在真菌状乳头的味觉细胞中观察到向内整流的C 1-通道蛋白C 1 C-2的免疫组织化学定位。结论是,在小鼠味觉细胞中,NaCl!诱导的应答的转导机制与KCl!诱导的应答的转导机制完全不同。

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