Gap junctional permeability is affected by cell volume changes and modulates volume regulation.
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.
Ngezahayo
A
A
University of Konstanz, Faculty of Biology, FRG.
Kolb
H A
HA
D000818:Animals; D002463:Cell Membrane Permeability; D003571:Cytochalasin B / Q000494:pharmacology; D004553:Electric Conductivity; D016244:Guanosine 5'-O-(3-Thiotriphosphate) / Q000494:pharmacology; D066298:In Vitro Techniques; D007365:Intercellular Junctions / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials; D051379:Mice; D008815:Mice, Inbred Strains; D009994:Osmolar Concentration; D010179:Pancreas / Q000166:cytology / Q000502:physiology*; D011112:Polymyxin B / Q000494:pharmacology
D016244:Guanosine 5'-O-(3-Thiotriphosphate); D003571:Cytochalasin B; D011112:Polymyxin B