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Potassium Dynamics in the Epileptic Cortex: New Insights on an Old Topic

Salk Institute for Biological Studies, Computational Neurobiology Laboratory, La Jolla, CA, Division of Biological Sciences, Section of Neurobiology, University of California San Diego, La Jolla

Maxim Bazhenov

Salk Institute for Biological Studies, Computational Neurobiology Laboratory, La Jolla, CA

Vicente Iragui-Madoz

Department of Neurosciences, University of California, San Diego, Neurology Service, VA San Diego Healthcare System, San Diego, CA

Terrence J. Sejnowski

Salk Institute for Biological Studies, Computational Neurobiology Laboratory, La Jolla, CA, Division of Biological Sciences, Section of Neurobiology, University of California San Diego, La Jolla, terry{at}salk.edu

The role of changes in the extracellular potassium concentration [K⁺]_o in epilepsy has remained unclear. Historically, it was hypothesized that [K⁺] _o is the causal factor for epileptic seizures. This so-called potassium accumulation hypothesis led to substantial debate but subsequently failed to find wide acceptance. However, recent studies on the pathophysiology of tissue from epileptic human patients and animal epilepsy models revealed aberrations in [K⁺]_o regulation. Computational models of cortical circuits that include ion concentration dynamics have catalyzed a renewed interest in the role of [K⁺]_o in epilepsy. The authors here connect classical and more recent insights on [K⁺] _o dynamics in the cortex with the goal of providing starting points for a next generation of [K⁺]_o research. Such research may ultimately lead to an entirely new class of antiepileptic drugs that act on the [K⁺]_o regulation system. NEUROSCIENTIST 14(5):422—433, 2008. DOI: 10.1177/1073858408317955

Key Words: Extracellular potassium concentration • Epilepsy • Neocortex • Hippocampus • Glia • Astrocytes • Dynamics • Computational model • Tonic-clonic seizures

The Neuroscientist, Vol. 14, No. 5, 422-433 (2008)
DOI: 10.1177/1073858408317955


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