A late slow depolarization unmasked in the presence of tetraethylammonium in neonatal rat sympathetic neurons in vitro.

Neonatal rat superior cervical ganglia were mechanically dissociated, and the sympathetic neurons grown in dispersed cell cultures. Intracellular microelectrodes were used to study the effects of tetraethylammonium (TEA+), a blocker of outward K+ currents, on the excitable properties of these neurons. Addition of TEA+ to the perfusion media (TEA+-media) caused the resting potential to depolarize and the action potential to increase in duration. In TEA+-media (20-60 mM), a late delayed depolarization (LDD) followed the falling phase of the action potential with a delay of 1.5-2 s (n = 95). The LDD peak amplitude was in the range of 4-26 mV and the duration, to full return of the resting potential, was in the range of 18-90 s. For a given cell the amplitude and duration of the LDD were constant. The LDD was associated with a conductance increase. No LDD could be elicited in the presence of calcium channel blockers. Evidence was found for a Ca2+-dependence of the LDD: increasing the extracellular Ca2+ concentration caused increases in the amplitude and duration of the LDD. The significance of an endogenous LDD-like potential and possible explanations for the origin of the LDD are discussed.