Effects of ion channel inhibitors on cold- and electrically-induced action potentials in Dionaea muscipula

Glass microelectrodes were inserted into Dionaea muscipula(Venus flytrap) lobes and the action potentials (APs) were recorded in response to a sudden temperature drop or a direct current (DC) application. The effect of potassium channel inhibitor, tetraethylammonium ion, was the lengthening of the depolarization phase of AP. APs were also affected by the anion channel inhibitor, anthracene-9-carboxylic acid, that made them slower and smaller. Neomycin, which disturbs inositol triphosphate-dependent Ca2+release, caused the visible inhibition of AP, too. Ruthenium red, which blocks cyclic ADP-ribose-dependent Ca2+release, totally inhibited DC-triggered APs and induced the decrease in the amplitudes of cold-evoked APs. Lanthanum ions significantly inhibited both cold- and DC-induced membrane potential changes. It was concluded that during excitation Dionaea muscipularelied upon the calcium influxes from both the extra- and intracellular compartments.Glass microelectrodes were inserted into Dionaea muscipula(Venus flytrap) lobes and the action potentials (APs) were recorded in response to a sudden temperature drop or a direct current (DC) application. The effect of potassium channel inhibitor, tetraethylammonium ion, was the lengthening of the depolarization phase of AP. APs were also affected by the anion channel inhibitor, anthracene-9-carboxylic acid, that made them slower and smaller. Neomycin, which disturbs inositol triphosphate-dependent Ca2+release, caused the visible inhibition of AP, too. Ruthenium red, which blocks cyclic ADP-ribose-dependent Ca2+release, totally inhibited DC-triggered APs and induced the decrease in the amplitudes of cold-evoked APs. Lanthanum ions significantly inhibited both cold- and DC-induced membrane potential changes. It was concluded that during excitation Dionaea muscipularelied upon the calcium influxes from both the extra- and intracellular compartments.