| First Author | Soh H | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 30382937 | Mgi Jnum | J:269758 |
| Mgi Id | MGI:6269199 | Doi | 10.7554/eLife.38617 |
| Citation | Soh H, et al. (2018) Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission. Elife 7:e38617 |
| abstractText | 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. |
