Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission

Elife. 2018 Nov 1;7:e38617. doi: 10.7554/eLife.38617.


KCNQ2/3 channels, ubiquitously expressed neuronal potassium channels, have emerged as indispensable regulators of brain network activity. Despite their critical role in brain homeostasis, the mechanisms by which KCNQ2/3 dysfunction lead to hypersychrony are not fully known. Here, we show that deletion of KCNQ2/3 channels changed PV+ interneurons', but not SST+ interneurons', firing properties. We also find that deletion of either KCNQ2/3 or KCNQ2 channels from PV+ interneurons led to elevated homeostatic potentiation of fast excitatory transmission in pyramidal neurons. Pvalb-Kcnq2 null-mice showed increased seizure susceptibility, suggesting that decreases in interneuron KCNQ2/3 activity remodels excitatory networks, providing a new function for these channels.

Keywords: KCNQ2; KCNQ3; epilepsy; interneurons; mouse; neuroscience; parvalbumin; potassium channels; seizure.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Female
  • Gene Deletion*
  • Homeostasis*
  • Interneurons / drug effects
  • Interneurons / metabolism*
  • KCNQ2 Potassium Channel / metabolism*
  • KCNQ3 Potassium Channel / metabolism*
  • Male
  • Mice
  • Potassium Channel Blockers / pharmacology
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / physiology
  • Synaptic Transmission* / drug effects


  • KCNQ2 Potassium Channel
  • KCNQ3 Potassium Channel
  • Potassium Channel Blockers