Details
| Original language | English |
|---|---|
| Pages (from-to) | 6-8 |
| Number of pages | 3 |
| Journal | FEBS letters |
| Volume | 276 |
| Issue number | 1-2 |
| Publication status | Published - 10 Dec 1990 |
Abstract
Isolated pancreatic acinar cell pairs became electrically uncoupled by exposure to a mild hypotonic shock. Reduction of bath osmolarity caused a delayed closure of gap junctional channels in the minute range. Dialysis of cell pairs by GTP[S] in the double whole-cell patch-clamp mode shortened the latency and shifted the hypotonically induced electrical uncoupling to lower osmolarity changes. Cellular treatment with cytochalasin B catalyzed electrical uncoupling by a hypotonic shock. In all cases, electrical uncoupling could be blocked completely by the protein kinase C (PKC) inhibitor polymyxin B. These results provide the first evidence suggesting that changes of cell volume and gap junctional permeability are correlated and that a G-protein dependent mechanism is involved. Evidence is presented that gap junctional coupling modulates volume regulation.
Keywords
- Animals, Cell Membrane Permeability, Cytochalasin B/pharmacology, Electric Conductivity, Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology, In Vitro Techniques, Intercellular Junctions/drug effects, Male, Membrane Potentials, Mice, Mice, Inbred Strains, Osmolar Concentration, Pancreas/cytology, Polymyxin B/pharmacology
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In: FEBS letters, Vol. 276, No. 1-2, 10.12.1990, p. 6-8.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Gap junctional permeability is affected by cell volume changes and modulates volume regulation
AU - Ngezahayo, A
AU - Kolb, H A
N1 - Funding information: Acknow/e&e~ents:T he authorsw ould like to thankD r Birgit Rose and Dr Roland Somogyif or helpful discussionsT. he work was supported by the Sonderforschungsbereich1 56 of the Deutsche Forschungsgemeinschaft.
PY - 1990/12/10
Y1 - 1990/12/10
N2 - Isolated pancreatic acinar cell pairs became electrically uncoupled by exposure to a mild hypotonic shock. Reduction of bath osmolarity caused a delayed closure of gap junctional channels in the minute range. Dialysis of cell pairs by GTP[S] in the double whole-cell patch-clamp mode shortened the latency and shifted the hypotonically induced electrical uncoupling to lower osmolarity changes. Cellular treatment with cytochalasin B catalyzed electrical uncoupling by a hypotonic shock. In all cases, electrical uncoupling could be blocked completely by the protein kinase C (PKC) inhibitor polymyxin B. These results provide the first evidence suggesting that changes of cell volume and gap junctional permeability are correlated and that a G-protein dependent mechanism is involved. Evidence is presented that gap junctional coupling modulates volume regulation.
AB - Isolated pancreatic acinar cell pairs became electrically uncoupled by exposure to a mild hypotonic shock. Reduction of bath osmolarity caused a delayed closure of gap junctional channels in the minute range. Dialysis of cell pairs by GTP[S] in the double whole-cell patch-clamp mode shortened the latency and shifted the hypotonically induced electrical uncoupling to lower osmolarity changes. Cellular treatment with cytochalasin B catalyzed electrical uncoupling by a hypotonic shock. In all cases, electrical uncoupling could be blocked completely by the protein kinase C (PKC) inhibitor polymyxin B. These results provide the first evidence suggesting that changes of cell volume and gap junctional permeability are correlated and that a G-protein dependent mechanism is involved. Evidence is presented that gap junctional coupling modulates volume regulation.
KW - Animals
KW - Cell Membrane Permeability
KW - Cytochalasin B/pharmacology
KW - Electric Conductivity
KW - Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
KW - In Vitro Techniques
KW - Intercellular Junctions/drug effects
KW - Male
KW - Membrane Potentials
KW - Mice
KW - Mice, Inbred Strains
KW - Osmolar Concentration
KW - Pancreas/cytology
KW - Polymyxin B/pharmacology
U2 - 10.1016/0014-5793(90)80493-3
DO - 10.1016/0014-5793(90)80493-3
M3 - Article
C2 - 2265713
VL - 276
SP - 6
EP - 8
JO - FEBS letters
JF - FEBS letters
SN - 0014-5793
IS - 1-2
ER -