Intracellular mechanism of ATP-induced depolarizing response in the bullfrog sympathetic ganglion cells.
Application of adenosine triphosphate (ATP) induced a depolarizing response in bullfrog sympathetic ganglion cells, which was associated with a decrease in membrane conductance. This depolarizing response was also produced by application of ADP, but not by adenosine, cyclic-AMP or cyclic-GMP. Suramin, an antagonist for the P2-purinoceptor, suppressed the response, while caffeine, an antagonist for the P1-purinoceptor, did not. Application of phospholipase C (PLC) inhibitors such as Li+ and 4-bromophenacyl bromide also suppressed the response. In addition, protein kinase C (PKC) inhibitors such as staurosporine and H-7 had a suppressant effect, while ryanodine, an inhibitor of Ca2 release, did not. These results suggest that ATP and ADP may stimulate P2-purinoceptor coupled with PLC, producing diacylglycerol, which activates PKC, resulting in the closing of K+ channel.
Department of Oral Physiology, Iwate Medical University School of Dentistry, Morioka, Japan.
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D000098:Acetophenones / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000818:Animals; D000969:Antinematodal Agents / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005728:Ganglia, Sympathetic / Q000187:drug effects*; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D011892:Rana catesbeiana; D018048:Receptors, Purinergic P2 / Q000502:physiology*; D019311:Staurosporine / Q000494:pharmacology; D013498:Suramin / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects*; D010738:Type C Phospholipases / Q000378:metabolism
D000098:Acetophenones; D000969:Antinematodal Agents; D004791:Enzyme Inhibitors; D018048:Receptors, Purinergic P2; D013498:Suramin; D000255:Adenosine Triphosphate; D008094:Lithium; D010738:Type C Phospholipases; D019311:Staurosporine; C006821:4-bromophenacyl bromide