RESURGENT SODIUM CURRENT AND ACTION-POTENTIAL FORMATION IN DISSOCIATED CEREBELLAR PURKINJE NEURONS

Voltage-dependent sodium channels were studied in dissociated cerebell ar Purkinje neurons from rats. In whole-cell recordings, a tetrodotoxi n (TTX)-sensitive inward current was elicited when the membrane was re polarized to voltages between -60 and -20 mV after depolarizations to +30 mV long enough to produce maximal inactivation. At -40 mV, this '' resurgent'' current peaked in 8 msec and decayed with a time constant of 30 msec. With 50 mM sodium as a charge carrier, the resurgent curre nt was on average similar to 120 pA. CA3 pyramidal neurons had no such current. The current may reflect recovery of inactivated channels thr ough open states, because in Purkinje neurons (but not CA3 neurons) th ere was partial recovery from inactivation at -40 mV, coinciding with the rise of resurgent current, In single-channel recordings, individua l channels gave openings corresponding to resurgent and conventional t ransient current. Action potentials were recorded from dissociated neu rons under current clamp to investigate the role of the resurgent curr ent in action potential formation. Purkinje neurons fired spontaneousl y at similar to 30 Hz. Hyperpolarization to -85 mV prevented spontaneo us firing, and brief depolarization then induced all-or-none firing of conglomerate action potentials comprising three to four spikes. When conglomerate action potentials were used as command voltages in voltag e-clamp experiments, mt-sensitive sodium current was elicited between spikes. The falling phase of an action potential is similar to voltage patterns that activate resurgent sodium current, and thus, resurgent sodium current likely contributes to the formation of conglomerate act ion potentials in Purkinje neurons.