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Volume 17, Number 12, Issue of June 15, 1997 pp. 4517-4526
Copyright ©1997 Society for Neuroscience

Resurgent Sodium Current and Action Potential Formation in Dissociated Cerebellar Purkinje Neurons

Received Jan. 30, 1997; revised March 22, 1997; accepted March 27, 1997.

Indira M. Raman and Bruce P. Bean

Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201, and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115

Voltage-dependent sodium channels were studied in dissociated cerebellar Purkinje neurons from rats. In whole-cell recordings, a tetrodotoxin (TTX)-sensitive inward current was elicited when the membrane was repolarized 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 current was on average ~120 pA. CA3 pyramidal neurons had no such current. The current may reflect recovery of inactivated channels through open states, because in Purkinje neurons (but not CA3 neurons) there was partial recovery from inactivation at 40 mV, coinciding with the rise of resurgent current. In single-channel recordings, individual channels gave openings corresponding to resurgent and conventional transient current. Action potentials were recorded from dissociated neurons under current clamp to investigate the role of the resurgent current in action potential formation. Purkinje neurons fired spontaneously at ~30 Hz. Hyperpolarization to 85 mV prevented spontaneous 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 voltage-clamp experiments, TTX-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 action potentials in Purkinje neurons.

Key words: sodium channel; Purkinje neuron; complex spike; afterdepolarization; tetrodotoxin; pacemaking; single channel; action potential; cerebellum

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				R. D. Smith and A. L. Goldin Functional Analysis of the Rat I Sodium Channel in Xenopus Oocytes J. Neurosci., February 1, 1998; 18(3): 811 - 820. [Abstract] [Full Text] [PDF]

				H. R. Parri and V. Crunelli Sodium Current in Rat and Cat Thalamocortical Neurons: Role of a Non-Inactivating Component in Tonic and Burst Firing J. Neurosci., February 1, 1998; 18(3): 854 - 867. [Abstract] [Full Text] [PDF]

				G. P. Ahern, S.-F. Hsu, V. A. Klyachko, and M. B. Jackson Induction of Persistent Sodium Current by Exogenous and Endogenous Nitric Oxide J. Biol. Chem., September 8, 2000; 275(37): 28810 - 28815. [Abstract] [Full Text] [PDF]

				S. R Williams, S. R Christensen, G. J Stuart, and M. Hausser Membrane potential bistability is controlled by the hyperpolarization-activated current IH in rat cerebellar Purkinje neurons in vitro J. Physiol., March 1, 2002; 539(2): 469 - 483. [Abstract] [Full Text] [PDF]

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