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Computational Model Predicts a Role for ERG Current in Repolarizing Plateau Potentials in Dopamine Neurons: Implications for Modulation of Neuronal Activity

¹Neuroscience Center and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana; ²Department of Physics and Astronomy, College of Charleston, Charleston, South Carolina;, ³Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee; and ⁴Maryland Psychiatric Research Center and the Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland

Submitted 13 April 2007; accepted in final form 10 August 2007

Blocking the small-conductance (SK) calcium-activated potassium channel promotes burst firing in dopamine neurons both in vivo and in vitro. In vitro, the bursting is unusual in that spiking persists during the hyperpolarized trough and frequently terminates by depolarization block during the plateau. We focus on the underlying plateau potential oscillation generated in the presence of both apamin and TTX, so that action potentials are not considered. We find that although the plateau potentials are mediated by a voltage-gated Ca²⁺ current, they do not depend on the accumulation of cytosolic Ca²⁺, then use a computational model to test the hypothesis that the slowly voltage-activated ether-a-go-go–related gene (ERG) potassium current repolarizes the plateaus. The model, which includes a material balance on calcium, is able to reproduce the time course of both membrane potential and somatic calcium concentration, and can also mimic the induction of plateau potentials by the calcium chelator BAPTA. The principle of separation of timescales was used to gain insight into the mechanisms of oscillation and its modulation using nullclines in the phase space. The model predicts that the plateau will be elongated and ultimately result in a persistent depolarization as the ERG current is reduced. This study suggests that the ERG current may play a role in burst termination and the relief of depolarization block in vivo.

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