Abstract
We found the voltage-gated K+ channel Kv12.2 to be a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 substantially reduced the firing threshold of these neurons. Kv12.2-/- (also known as Kcnh3-/-) mice showed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Action Potentials / physiology
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Animals
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Cell Line
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Cells, Cultured
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Convulsants / toxicity
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Epilepsy / chemically induced
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Epilepsy / genetics
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Epilepsy / physiopathology*
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Ether-A-Go-Go Potassium Channels / antagonists & inhibitors
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Ether-A-Go-Go Potassium Channels / genetics
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Ether-A-Go-Go Potassium Channels / metabolism*
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Female
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Hippocampus / drug effects
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Hippocampus / physiopathology*
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Humans
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In Vitro Techniques
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Male
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Neurons / drug effects
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Neurons / physiology*
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Pentylenetetrazole / toxicity
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiopathology
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Seizures / chemically induced
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Seizures / genetics
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Seizures / physiopathology
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Video Recording
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Xenopus
Substances
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Convulsants
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Ether-A-Go-Go Potassium Channels
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Kcnh3 protein, mouse
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Pentylenetetrazole