In vertebrate embryos gap junctional conductance (g(j)) is reduced by transjunctional voltage (V(j)) 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 V(j) and intracellular pH (pH(i)) gate g(j) are apparently independent. Partial reduction of g(j) by lowering pH(i) neither attenuates nor enhances further reduction by V(j). Certain drugs irreversibly (glutaraldehyde, 1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline) or reversible (retinolic acid) abolish dependence of g(j) on pH(i) without appreciably affecting kinetic properties of voltage dependence or the shape of the steady-state V(j)-g(j) relation. These findings suggest that the mechanisms by which pH(i) and V(j) act on the gap junction are at least partially distinct and presumably involve separate regions of the junctional macromolecules.
|Original language||English (US)|
|Number of pages||4|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - 1986|
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