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

Heun Soh, Suhyeorn Park, Kali Ryan, Kristen Springer, Atul Maheshwari, Anastasios V. Tzingounis

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article numbere38617
JournaleLife
Volume7
DOIs
StatePublished - Nov 1 2018
Externally publishedYes

ASJC Scopus subject areas

  • General Neuroscience
  • General Immunology and Microbiology
  • General Biochemistry, Genetics and Molecular Biology

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