Comparison of activation of non-selective cation channels by protein kinase-A in guinea-pig and mouse pancreatic acinar cells.
The effects of cyclic AMP-dependent protein kinase (PKA) on non-selective cation (NSC) channels in the plasma membrane of guinea-pig and mouse pancreatic acinar cells were studied by patch-clamp single-channel techniques. In both species, ATP (1.4 mM) acting on the inside of the membrane (Ca2+ concentration, 10(-6)M) inhibited the opening of the NSC channel with a unit conductance of 25 pS. The addition of a catalytic unit of PKA (25 U/ml) in the presence of ATP to the inside of guinea-pig cells evoked an opening of a new channel, which is a Ca(2+)-activated and voltage-sensitive NSC channel with a unit conductance of about 45 pS (in symmetrical monovaleńt cation-rich solution). On the other hand, 25 pS Ca(2+)-activated NSC channel in mouse cells was re-opened by identical PKA application. The application of PKA-inhibitor did not activate NSC channels in either species. The addition of 10(-6)M ACh to the bath solution containing 10(-6)M insulin, whose addition with ACh has been reported to increase cAMP, evoked a marked and sustained increase in the opening of the guinea-pig 45 pS or the mouse 25 pS NSC channel in intact cells (cell-attached configurations). This was not seen in the absence of insulin. These results suggest that the cAMP-dependent mechanism in the pancreatic acinar cells can activate NSC channels in the presence of ATP on the inside of the cell.
Suzuki
K
K
Department of Bio-Medical Engineering, School of High-Technology for Human Welfare, Tokai University, Numazu, Japan.
Koyama
I
I
D000818:Animals; D002412:Cations / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000494:pharmacology*; D006168:Guinea Pigs; D007473:Ion Channels / Q000187:drug effects*; D007700:Kinetics; D051379:Mice; D008815:Mice, Inbred Strains; D010179:Pancreas / Q000187:drug effects*; D018408:Patch-Clamp Techniques
D002412:Cations; D007473:Ion Channels; D017868:Cyclic AMP-Dependent Protein Kinases