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EDITORIAL FOCUS
). Resurgent currents were first described in Purkinje cells where they improve high-frequency firing (Raman and Bean 1997). More recently, resurgent currents have also been implicated in rhythmic firing of neurons in the subthalamic nucleus, an area gaining importance in the treatment of end-stage Parkinson's syndromes (Do and Bean 2003). Few neurons throughout the brain, however, are known to display resurgent currents, suggesting that these currents are carried by a select subset of Na+ channels. Compelling evidence that this subset corresponds to one particular Na+ channel subunit is the finding that Purkinje cells lacking Nav1.6 alpha subunits (med mutant) do not display resurgent currents. However, under conditions of artificially induced slowing of inactivation by beta-pompilidotoxin, the remaining Na+ channels could be made to produce a resurgent current (Grieco and Raman 2004). The report by Do and Bean (this issue, p. 726–733) sheds further light on this story. By identifying resurgent current in subthalamic nucleus neurons from mice lacking the Nav1.6 alpha subunits, they demonstrate that resurgent current is not a property unique to Nav1.6 subunits. Do and Bean's findings suggest instead that some form of modulation or an association with an auxiliary subunit, rather than the specific alpha subunit, is critical for the production of resurgent current. Such an association would need to produce a secondary inactivation to compete with classical fast inactivation. Whatever the nature of this putative element, different classes of neurons may rely on different Na+ channel alpha-subunits to produce resurgent currents. Resurgent currents may indeed represent a more ubiquitous determinant of cell-specific firing than we now appreciate.
Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5513
Address for reprint requests and other correspondence: Dept. of Biology and Biochemistry, University of Houston, 4800 Calhoun Rd., Houston TX, 77204-5513 (E-mail: ccolbert{at}uh.edu).
REFERENCES
Do MT and Bean BP. Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice. J Neurophysiol 92: 726–733, 2004.
Do MT and Bean BP. Subthreshold sodium currents and pacemaking of subthalamic neurons: modulation by slow inactivation. Neuron 39: 109–120, 2003.[CrossRef][ISI][Medline]
Grieco TM and Raman IM. Production of resurgent current in NaV1.6-null Purkinje neurons by slowing sodium channel inactivation with beta-pompilidotoxin. J Neurosci 24: 35–42, 2004.
Raman IM and Bean BP. Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms. Biophys J 80: 729–737, 2001.
Raman IM and Bean BP. Resurgent sodium current and action potential formation in dissociated cerebellar Purkinje neurons. J Neurosci 17: 4517–4526, 1997.
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