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

eLife | 2018

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.

Pubmed ID: 30382937 RIS Download

Research resources used in this publication

Associated grants

  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL137094
  • Agency: NIH HHS, United States
    Id: NS101596
  • Agency: NINDS NIH HHS, United States
    Id: R56 NS073981
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS101596
  • Agency: NIH HHS, United States
    Id: NS096029
  • Agency: NIH HHS, United States
    Id: NS073981
  • Agency: NINDS NIH HHS, United States
    Id: K08 NS096029

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