Calcium‐dependent potentials in the mammalian sympathetic neurone.

Abstract

Intracellular recordings from post-ganglionic neurons of the rat superior cervical ganglion revealed 2 non-synaptic potentials dependent upon Ca2+, a hyperpolarizing afterpotential (HAP) and a tetrodotoxin (TTX)-insensitive spike. The HAP followed regenerative discharge of the membrane potential in normal and TTX-containing Locke solution. The HAP appeared to arise from an increased K+ conductance because it was associated with a decrease in input resistance, reversed at -90 mV, and was proportional in magnitude to the extracellular K+ concentration. Tetraethylammonium (TEA) and 4-aminopyridine (4-AP) apparently antagonized a voltage-sensitive K+ conductance because they broadened the action potential. These substances reduced only slightly the peak amplitude and earliest phases of the HAP. The TTX-insensitive spike was most apparent when TEA was present and was invariably followed by an HAP with a magnitude proportional to that of the spike. The magnitude of the HAP and the TTX-insensitive spike was directly proportional to the external Ca2+ concentration and was antagonized by Co2+ and Mn2+ in a dose-dependent fashion. In normal Locke solution, Ba2+ antagonized the HAP and allowed the neuron to sustain discharge during prolonged depolarization. In Locke solution containing TTX and TEA, Ba2+ reduced the magnitude of the HAP but greatly increased the duration of the TTX-insensitive spike. The HAP was not significantly affected by altering external Cl- concentration and the TTX-insensitive spike was not reduced by altering external Na+ concentration. The post-ganglionic neuron supports a regenerative Ca2+ conductance mechanism which in turn triggers an increased K+ conductance. The HAP appears to result from outward K+ current in both a Ca2+ and voltage-dependent fashion.