Effect of calcium on synaptic facilitation by potassium channel blockers in superior cervical ganglion of rat.

The effects of potassium channel blockers on synaptic transmission were studied in the isolated superior cervical ganglia of the rat by means of extracellular recordings. The ganglia were exposed to gradual increase in the concentration of calcium in the presence and absence of potassium channel blockers. At all levels of calcium (0.1-2 mM), 4-aminopyridine (4-AP) produced marked potentiation of both amplitude and duration of the compound action potential. At 0.1 mM, 4-AP completely reversed the failure of transmission regularly seen in low calcium (0.1 mM). The increase in duration, measured as time to peak, was more pronounced in low calcium and became less marked as the concentration of calcium was raised. In media containing low concentrations of calcium (0.8 mM), 4-AP induced a massive spontaneous discharge, often with rhythmic bursts. Cesium (6 mM) abolished the action potential in low calcium media, however, increasing levels of calcium in the presence of cesium resulted in recovery and later marked potentiation of both the amplitude and duration of the action potential in a calcium concentration-dependent manner. Guanidine potentiated the amplitude of the compound action potential but had no measurable effect on its duration and was unable to reverse transmission failure in low calcium. No potentiation of the amplitude or duration of the action potential was seen with tetraethylammonium. Neither guanidine nor tetraethylammonium induced a spontaneous discharge. The results suggest that some actions of 4-AP are unrelated to blockade of potassium channels.