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...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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eLife Sciences Publications Ltd
2018-11-01
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| Series: | eLife |
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| Online Access: | https://elifesciences.org/articles/38617 |
| _version_ | 1818028547466330112 |
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| author | Heun Soh Suhyeorn Park Kali Ryan Kristen Springer Atul Maheshwari Anastasios V Tzingounis |
| author_facet | Heun Soh Suhyeorn Park Kali Ryan Kristen Springer Atul Maheshwari Anastasios V Tzingounis |
| author_sort | Heun Soh |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-10T05:05:32Z |
| format | Article |
| id | doaj.art-d16027a3671742edbdf3ca130993bf7e |
| institution | Directory Open Access Journal |
| issn | 2050-084X |
| language | English |
| last_indexed | 2024-12-10T05:05:32Z |
| publishDate | 2018-11-01 |
| publisher | eLife Sciences Publications Ltd |
| record_format | Article |
| series | eLife |
| spelling | doaj.art-d16027a3671742edbdf3ca130993bf7e2022-12-22T02:01:15ZengeLife Sciences Publications LtdeLife2050-084X2018-11-01710.7554/eLife.38617Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmissionHeun Soh0Suhyeorn Park1Kali Ryan2Kristen Springer3Atul Maheshwari4https://orcid.org/0000-0003-3045-7901Anastasios V Tzingounis5https://orcid.org/0000-0002-4605-3437Department of Physiology and Neurobiology, University of Connecticut, Connecticut, United StatesDepartment of Neurology, Baylor College of Medicine, Texas, United StatesDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United StatesDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United StatesDepartment of Neurology, Baylor College of Medicine, Texas, United StatesDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United StatesKCNQ2/3 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.https://elifesciences.org/articles/38617potassium channelsKCNQ2KCNQ3interneuronsepilepsyseizure |
| spellingShingle | Heun Soh Suhyeorn Park Kali Ryan Kristen Springer Atul Maheshwari Anastasios V Tzingounis Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission eLife potassium channels KCNQ2 KCNQ3 interneurons epilepsy seizure |
| title | Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission |
| title_full | Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission |
| title_fullStr | Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission |
| title_full_unstemmed | Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission |
| title_short | Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission |
| title_sort | deletion of kcnq2 3 potassium channels from pv interneurons leads to homeostatic potentiation of excitatory transmission |
| topic | potassium channels KCNQ2 KCNQ3 interneurons epilepsy seizure |
| url | https://elifesciences.org/articles/38617 |
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