Spray D C, Campos de Carvalho A, Bennett M V
Proc Natl Acad Sci U S A. 1986 May;83(10):3533-6. doi: 10.1073/pnas.83.10.3533.
In vertebrate embryos gap junctional conductance (gj) is reduced by transjunctional voltage (Vj) and by cytoplasmic acidification; in each case sensitivity is comparable to those of other channels gated by voltage and ligand-receptor binding. We show here that the mechanisms by which Vj and intracellular pH (pHi) gate gj are apparently independent. Partial reduction of gj by lowering pHi neither attenuates nor enhances further reduction by Vj. Certain drugs irreversibly (glutaraldehyde, 1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline) or reversibly (retinoic acid) abolish dependence of gj on pHi without appreciably affecting kinetic properties of voltage dependence or the shape of the steady-state Vj-gj relation. These findings suggest that the mechanisms by which pHi and Vj act on the gap junction are at least partially distinct and presumably involve separate regions of the junctional macromolecules.
在脊椎动物胚胎中，间隙连接电导（gj）会因跨连接电压（Vj）和细胞质酸化而降低；在每种情况下，其敏感性与其他由电压和配体-受体结合门控的通道相当。我们在此表明，Vj和细胞内pH（pHi）门控gj的机制显然是独立的。通过降低pHi部分降低gj，既不会减弱也不会增强Vj进一步降低gj的作用。某些药物不可逆地（戊二醛、1-乙氧羰基-2-乙氧基-1,2-二氢喹啉）或可逆地（视黄酸）消除gj对pHi的依赖性，而不会明显影响电压依赖性的动力学特性或稳态Vj-gj关系的形状。这些发现表明，pHi和Vj作用于间隙连接的机制至少部分不同，并且可能涉及连接大分子的不同区域。
