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 language | English (US) |
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Article number | e38617 |
Journal | eLife |
Volume | 7 |
DOIs | |
State | Published - Nov 1 2018 |
Externally published | Yes |
ASJC Scopus subject areas
- General Neuroscience
- General Immunology and Microbiology
- General Biochemistry, Genetics and Molecular Biology