KCNQ5 Kþ channels control hippocampal synaptic inhibition and fast network oscillations

By February 4, 2015

Publication Details

Featured Authors

Pawel Fidzinski Thomas J. Jentsch
Acute Mouse Hippocampus Single unit Penetrating Electrode A1x32-6mm50-413|A4x8-5mm-200-400-413

KCNQ2 (Kv7.2) and KCNQ3 (Kv7.3) Kþ 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.

Nat Commun. 2015 Feb 4;6:6254. doi: 10.1038/ncomms7254.

http://www.ncbi.nlm.nih.gov/pubmed/25649132 February 4, 2015 Leibniz-Institut fur Molekulare Pharma