Sensitivity of gap junctional conductance to H ions in amphibian embryonic cells is independent of voltage sensitivity

David C. Spray, A. C. Campos De Carvalho, Michael V. L. Bennett

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10 Citations (Scopus)

Abstract

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 languageEnglish (US)
Pages (from-to)3533-3536
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume83
Issue number10
StatePublished - 1986

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Amphibians
Ions
Ligand-Gated Ion Channels
Gap Junctions
Glutaral
Vertebrates
Embryonic Structures
Acids
Pharmaceutical Preparations

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

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abstract = "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.",
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T1 - Sensitivity of gap junctional conductance to H ions in amphibian embryonic cells is independent of voltage sensitivity

AU - Spray, David C.

AU - Campos De Carvalho, A. C.

AU - Bennett, Michael V. L.

PY - 1986

Y1 - 1986

N2 - 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.

AB - 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.

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