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

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 the

SUBMITTER: Soh H 

PROVIDER: S-EPMC6211828 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature