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

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 deleti...

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Bibliographic Details
Published in:eLife 2018-11, Vol.7
Main Authors: Soh, Heun, Park, Suhyeorn, Ryan, Kali, Springer, Kristen, Maheshwari, Atul, Tzingounis, Anastasios V
Format: Article
Language:English
Subjects:
Animals
epilepsy
Female
Gene Deletion
Homeostasis
Hybridization
Interneurons
Interneurons - drug effects
Interneurons - metabolism
KCNQ2
KCNQ2 Potassium Channel - metabolism
KCNQ2 protein
KCNQ3
KCNQ3 Potassium Channel - metabolism
Male
Mice
Neurons
Neuroscience
Neurosciences
Potassium
Potassium Channel Blockers - pharmacology
Potassium channels
Potassium channels (voltage-gated)
Potentiation
Pyramidal cells
Pyramidal Cells - drug effects
Pyramidal Cells - physiology
seizure
Seizures (Medicine)
Short Report
Synaptic Transmission - drug effects
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Description
Summary: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. null-mice showed increased seizure susceptibility, suggesting that decreases in interneuron KCNQ2/3 activity remodels excitatory networks, providing a new function for these channels.
ISSN:2050-084X
2050-084X
DOI:10.7554/eLife.38617