KCNQ5 K+ channels control hippocampal synaptic inhibition and fast network oscillations

Pawel Fidzinski, Tatiana Korotkova, Matthias Heidenreich, Nikolaus Maier, Sebastian Schuetze, Oliver Kobler, Werner Zuschratter, Dietmar Schmitz, Alexey Ponomarenko () and Thomas J. Jentsch ()
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Pawel Fidzinski: Leibniz-Institut für Molekulare Pharmakologie (FMP)
Tatiana Korotkova: Leibniz-Institut für Molekulare Pharmakologie (FMP)
Matthias Heidenreich: Leibniz-Institut für Molekulare Pharmakologie (FMP)
Nikolaus Maier: Neurowissenschaftliches Forschungszentrum, Charité Universitätsmedizin
Sebastian Schuetze: Leibniz-Institut für Molekulare Pharmakologie (FMP)
Oliver Kobler: Leibniz-Institut für Neurobiologie (LIN)
Werner Zuschratter: Leibniz-Institut für Neurobiologie (LIN)
Dietmar Schmitz: NeuroCure Cluster of Excellence, Charité Universitätsmedizin
Alexey Ponomarenko: Leibniz-Institut für Molekulare Pharmakologie (FMP)
Thomas J. Jentsch: Leibniz-Institut für Molekulare Pharmakologie (FMP)

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract KCNQ2 (Kv7.2) and KCNQ3 (Kv7.3) K+ channels dampen neuronal excitability and their functional impairment may lead to epilepsy. Less is known about KCNQ5 (Kv7.5), which also displays wide expression in the brain. Here we show an unexpected role of KCNQ5 in dampening synaptic inhibition and shaping network synchronization in the hippocampus. KCNQ5 localizes to the postsynaptic site of inhibitory synapses on pyramidal cells and in interneurons. Kcnq5dn/dn mice lacking functional KCNQ5 channels display increased excitability of different classes of interneurons, enhanced phasic and tonic inhibition, and decreased electrical shunting of inhibitory postsynaptic currents. In vivo, loss of KCNQ5 function leads to reduced fast (gamma and ripple) hippocampal oscillations, altered gamma-rhythmic discharge of pyramidal cells and impaired spatial representations. Our work demonstrates that KCNQ5 controls excitability and function of hippocampal networks through modulation of synaptic inhibition.

Date: 2015
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DOI: 10.1038/ncomms7254

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