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

eLife

Suhyeorn Park¹  Atul Maheshwari¹  Kali Ryan²  Kristen Springer²  Anastasios V Tzingounis²  Heun Soh² 

[1] Department of Neurology, Baylor College of Medicine, Texas, United States;Department of Physiology and Neurobiology, University of Connecticut, Connecticut, United States;

关键词: potassium channels;    KCNQ2;    KCNQ3;    interneurons;    epilepsy;    seizure;   

DOI  :  10.7554/eLife.38617

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown