Effects of K+-channel blockers on transmitter release in bullfrog sympathetic ganglia

Effects of K+-channel blockers, tetraethylammonium (TEA), 4-aminopyridine (4-AP) and Cs+ on synaptic transmission were studied with an intracellular electrode in bullfrog sympathetic ganglia. TEA (25-500 microM), 4-AP (0.6-5 microM) and Cs+ (50 microM-10 mM) all increased the quantal content of the fast excitatory postsynaptic potential in a dose-dependent manner. The effects of TEA were rapid in onset and recovery, whereas those of 4-AP and Cs+ appeared with a notable delay and reversed slowly. All blockers lengthened synaptic delay. When compared at approximately equipotent concentrations for potentiation of transmitter release, TEA and 4-AP were found to produce a similar lengthening of the synaptic delay whereas Cs+ caused a much greater prolongation. The quantal size of the fast excitatory postsynaptic potential and the amplitude of the acetylcholine potential were not affected by 4-AP or Cs+, but were depressed by TEA. These results indicate that TEA, 4-AP and Cs+ enhance evoked transmitter release in bullfrog sympathetic ganglia. It is suggested that the potentiation is caused, at least in part, by a mechanism that increases Ca++ influx in the nerve terminal. The enhanced influx is presumed to be mediated by a broadening of the presynaptic action potential after K+-channel blockade.