Policing the ball: a new potassium channel subunit determines inactivation rate.
Inactivation of potassium currents during maintained firing results in a progressive increase in action potential width and neuronal excitability. In Kv1.1 channels, inactivation has attributed to a beta subunit that blocks the pore of the channel shortly after channel opening. In this issue of Neuron, Shulte and colleagues have identified a novel channel subunit whose interaction with Kv1.1 and the beta subunit prevents such inactivation. Mutations in this subunit lead to temporal lobe epilepsy.
Kaczmarek
Leonard K
LK
Department of Pharmacology and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
D000818:Animals; D006801:Humans; D051663:Kv1.2 Potassium Channel / Q000737:chemistry / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D008954:Models, Biological; D009433:Neural Inhibition / Q000502:physiology*; D021122:Protein Subunits / Q000502:physiology*
D051663:Kv1.2 Potassium Channel; D021122:Protein Subunits