Modulatory actions of ATP on membrane potentials of bullfrog sympathetic ganglion cells.
Adenosine triphosphate (ATP) depolarized the membrane of bullfrog sympathetic ganglion cells by decreasing resting K+ conductance. ATP also depressed the maximum amplitude of after-hyperpolarization of action potentials. Voltage-clamp study revealed that ATP markedly suppressed the TEA-insensitive K+ current which appeared to correspond to the M-current, while it affected less significantly on the delayed rectifier K+ current. It was suggested that ATP depolarized resting membrane by suppressing resting K+ conductances, including the M-current, and also depressed the after-hyperpolarization of action potentials by suppressing both the M-current and delayed rectifier K+ current.
D000200:Action Potentials / Q000187:drug effects; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000249:Adenosine Monophosphate / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D005728:Ganglia, Sympathetic / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D011892:Rana catesbeiana; D013779:Tetrodotoxin / Q000494:pharmacology
D000249:Adenosine Monophosphate; D013779:Tetrodotoxin; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D011188:Potassium