CALCIUM-DEPENDENT POTENTIALS IN THE MAMMALIAN SYMPATHETIC NEURON

1. Intracellular recordings from post‐ganglionic neurones of the rat superior cervical ganglion revealed two non‐synaptic potentials dependent upon Ca2+, a hyperpolarizing afterpotential (h.a.p.) and a tetrodotoxin (TTX)‐insensitive spike. 2. The h.a.p. followed regeneration discharge of the membrane potential in normal and TTX‐containing Locke solution. 3. The h.a.p. 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. 4. Tetraethylammonium (TEA) and 4‐aminopyridine (4‐AP) apparently antagonized a voltage‐sensitive K+ conductance because they broadened the action potential. However, these substances reduced only slightly the peak amplitude and earliest phases of the h.a.p. 5. The TTX‐insensitive spike was most apparent when TEA was present and was invariably followed by an h.a.p. with a magnitude proportional to that of the spike. 6. The magnitude of the h.a.p. 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. 7. In normal Locke solution, Ba2+ antagonized the h.a.p. and allowed the neurone to sustain discharge during prolonged depolarization. In Locke solution containing TTX and TEA, Ba2+ reduced the magnitude of the h.a.p. but greatly increased the duration of the TTX‐insensitive spike. 8. The h.a.p. was not significantly affected by altering external Cl‐ concentration and the TTX‐insensitive spike was not reduced by altering external Na+ concentration. 9. It is concluded that the post‐ganglionic neurone supports a regenerative Ca2+ conductance mechanism which in turn triggers an increased K+ conductance. The h.a.p. appears to result from outward K+ current in both a Ca2+ and voltage‐dependent fashion. © 1979 The Physiological Society