Calcium-dependent potentials in the mammalian sympathetic neurone.

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.