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

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  • Pawel Fidzinski

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    Max-Delbrück-Centrum für Molekulare Medizin (MDC)
    Klinik für Neurologie, Charité Universitätsmedizin)

  • Tatiana Korotkova

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    NeuroCure Cluster of Excellence, Charité Universitätsmedizin)

  • Matthias Heidenreich

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    Max-Delbrück-Centrum für Molekulare Medizin (MDC)
    Present address: Broad Institute, 415 Main Street, Cambridge, Massachusetts 02142, USA)

  • Nikolaus Maier

    (Neurowissenschaftliches Forschungszentrum, Charité Universitätsmedizin)

  • Sebastian Schuetze

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    Max-Delbrück-Centrum für Molekulare Medizin (MDC))

  • Oliver Kobler

    (Leibniz-Institut für Neurobiologie (LIN))

  • Werner Zuschratter

    (Leibniz-Institut für Neurobiologie (LIN))

  • Dietmar Schmitz

    (NeuroCure Cluster of Excellence, Charité Universitätsmedizin
    Neurowissenschaftliches Forschungszentrum, Charité Universitätsmedizin
    Deutsches Zentrum für Neurodegenerative Erkrankungen in der Helmholtz-Gemeinschaft (DZNE), Charité Universitätsmedizin)

  • Alexey Ponomarenko

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    NeuroCure Cluster of Excellence, Charité Universitätsmedizin)

  • Thomas J. Jentsch

    (Leibniz-Institut für Molekulare Pharmakologie (FMP)
    Max-Delbrück-Centrum für Molekulare Medizin (MDC)
    NeuroCure Cluster of Excellence, Charité Universitätsmedizin)

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.

Suggested Citation

  • Pawel Fidzinski & Tatiana Korotkova & Matthias Heidenreich & Nikolaus Maier & Sebastian Schuetze & Oliver Kobler & Werner Zuschratter & Dietmar Schmitz & Alexey Ponomarenko & Thomas J. Jentsch, 2015. "KCNQ5 K+ channels control hippocampal synaptic inhibition and fast network oscillations," Nature Communications, Nature, vol. 6(1), pages 1-13, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7254
    DOI: 10.1038/ncomms7254
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