The electrogenesis of adrenaline-hyperpolarization of sympathetic ganglion cells in bullfrogs.
Bullfrog sympathetic ganglion cells produced hyperpolarizing (Ad-hyperpolarization) and depolarizing (Ad-depolarization) responses when adrenaline (Ad) was directly applied to ganglia. The nature of Ad-hyperpolarization recorded by the sucrose-gap method was analysed in the present experiment, in order to clarify its electrogenesis. The amplitude of Ad-hyperpolarization was increased or decreased while ganglion cell membranes were hyperpolarized or depolarized, respectively, by applying a moderate conditioning current to the ganglia. The Ad-hyperpolarization was depressed in K+-rich solutions as well as in K+-deficient solutions. It was not significantly altered by replacing the extracellular total Cl ions by equimolar glutamate or thiosulfate ions. Ad-hyperpolarization was depressed and finally abolished in the Na+-free Tris solution, and was reversibly eliminated in the solution where Na ions were totally replaced by equimolar Li ions. It was enhanced when a preparation was previously perfused in the K+-free, Na+-rich solution for certain periods, during which the intracellular Na+ concentration might be increased. Ad-hyperpolarization was depressed by lowering the temperature and by the action of ouabain, and the amplitude of Ad-hyperpolarization was markedly increased in the presence of TEA. The ionic mechanism underlying the generation of Ad-hyperpolarization was discussed on the basis of these present experimental results, and it was suggested that Ad-hyperpolarization might be generated by an electrogenic sodium pump.
The electrogenesis of adrenaline-hyperpolarization of sympathetic ganglion cells in bullfrogs. Bullfrog sympathetic ganglion cells produced hyperpolarizing (Ad-hyperpolarization) and depolarizing (Ad-depolarization) responses when adrenaline (Ad) was directly applied to ganglia. The nature of Ad-hyperpolarization recorded by the sucrose-gap method was analysed in the present experiment, in order to clarify its electrogenesis. The amplitude of Ad-hyperpolarization was increased or decreased while ganglion cell membranes were hyperpolarized or depolarized, respectively, by applying a moderate conditioning current to the ganglia. The Ad-hyperpolarization was depressed in K+-rich solutions as well as in K+-deficient solutions. It was not significantly altered by replacing the extracellular total Cl ions by equimolar glutamate or thiosulfate ions. Ad-hyperpolarization was depressed and finally abolished in the Na+-free Tris solution, and was reversibly eliminated in the solution where Na ions were totally replaced by equimolar Li ions. It was enhanced when a preparation was previously perfused in the K+-free, Na+-rich solution for certain periods, during which the intracellular Na+ concentration might be increased. Ad-hyperpolarization was depressed by lowering the temperature and by the action of ouabain, and the amplitude of Ad-hyperpolarization was markedly increased in the presence of TEA. The ionic mechanism underlying the generation of Ad-hyperpolarization was discussed on the basis of these present experimental results, and it was suggested that Ad-hyperpolarization might be generated by an electrogenic sodium pump.