{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T15:00:55Z","timestamp":1790780455816,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:00:00Z","timestamp":1790726400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:00:00Z","timestamp":1790726400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000025","name":"National Institute of Mental Health","doi-asserted-by":"publisher","award":["5T32MH112510"],"award-info":[{"award-number":["5T32MH112510"]}],"id":[{"id":"10.13039\/100000025","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R21 NS123459"],"award-info":[{"award-number":["R21 NS123459"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009633","name":"Eunice Kennedy Shriver National Institute of Child Health and Human Development","doi-asserted-by":"publisher","award":["P50 HD105351"],"award-info":[{"award-number":["P50 HD105351"]}],"id":[{"id":"10.13039\/100009633","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      \u03b3\u2010Aminobutyric acidergic (GABAergic) parvalbumin\u2010positive (PV+) interneurons are critical for maintaining cortical inhibitory tone, with their dysfunction predictably leading to epilepsy. Rapid PV+ interneuron firing is essential for their normal function and is maintained in part by potassium voltage\u2010gated channels. Specifically, the Kv3.1 voltage\u2010gated potassium channel, which is highly expressed in PV+ interneurons, is essential for maintenance of rapid PV+ interneuron firing. However, whether Kv3.1 expression is modulated by repeated seizures is unknown. Given Kv3.1's role in PV+ cell biology, we tested (1) whether Kv3.1 expression is affected by recurrent seizures and (2) whether Kv3.1\u2010positive allosteric modulation suppresses either chemoconvulsant seizures or spontaneous seizures in an\n                      <jats:italic>Scn1a<\/jats:italic>\n                      haploinsufficient (\n                      <jats:italic>Scn1a<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>+\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      ) Dravet syndrome mouse model, which is characterized by PV+ cell dysfunction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Seizure threshold was measured in adult wild\u2010type mice by pentylenetetrazole (PTZ) challenge. In juvenile\n                      <jats:italic>Scn1a<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>+\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      mice, we measured threshold for hyperthermia\u2010induced seizures, and in adult\n                      <jats:italic>Scn1a<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>+\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      mice spontaneous seizures were recorded by video\u2010EEG. To test whether seizures alter Kv3.1 expression, cortical tissue was harvested after seizure induction or monitoring for spontaneous seizures, and Kv3.1 protein expression was measured by immunoblot and by immunohistochemistry. As a test of Kv3.1 contribution to seizure control, mice in each group were treated with a tool Kv3.1\u2010positive allosteric modulator, AUT1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Kv3.1 protein was reduced in the cortex of mice with either spontaneous or PTZ\u2010induced seizures. Moreover, Kv3.1 protein was decreased in PV+ interneurons and mislocalized to the cytoplasm rather than the cell membrane in seizing\n                      <jats:italic>Scn1a<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>+\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      mice. Kv3.1 potentiation by AUT1 attenuated three different types of seizures\u2014chemically induced, thermally induced, and spontaneous\u2014in juvenile and adult mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>These data highlight the Kv3.1 role as (1) an element of seizure control that declines after recurrent seizures and (2) a potential novel therapeutic target for seizure control in Dravet syndrome and other epilepsies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/epi.70511","type":"journal-article","created":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T14:45:17Z","timestamp":1790779517000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Kv3.1 activation suppresses provoked and spontaneous seizures in a mouse Dravet syndrome model"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7020-8347","authenticated-orcid":false,"given":"Sheryl Anne D.","family":"Vermudez","sequence":"first","affiliation":[{"name":"Department of Neurology and F.M. 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Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-7596-7509","authenticated-orcid":false,"given":"Gabrielle E.","family":"McGinty","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-2271-8328","authenticated-orcid":false,"given":"Amanda M.","family":"Liebhardt","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-1798-2927","authenticated-orcid":false,"given":"Rui","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-3549-8286","authenticated-orcid":false,"given":"Benjamin","family":"Hui","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yini","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-4961-0819","authenticated-orcid":false,"given":"David J.","family":"Arce","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4975-7330","authenticated-orcid":false,"given":"Henry H. C.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7044-2953","authenticated-orcid":false,"given":"Mustafa","family":"Sahin","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Rosamund Stone Zander Hansjoerg Wyss Translational Neuroscience Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6495-5928","authenticated-orcid":false,"given":"Alexander","family":"Rotenberg","sequence":"additional","affiliation":[{"name":"Department of Neurology and F.M. Kirby Neurobiology Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Neurology, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"},{"name":"Rosamund Stone Zander Hansjoerg Wyss Translational Neuroscience Center, Boston Children's Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,30]]},"reference":[{"issue":"8","key":"e_1_2_12_2_1","doi-asserted-by":"crossref","DOI":"10.1523\/JNEUROSCI.1169-24.2024","article-title":"Synaptic vesicle glycoprotein 2A knockout in parvalbumin and somatostatin interneurons drives seizures in the postnatal mouse brain","volume":"45","author":"Bartholome O","year":"2025","journal-title":"J Neurosci"},{"key":"e_1_2_12_3_1","doi-asserted-by":"crossref","DOI":"10.1016\/j.expneurol.2024.114962","article-title":"A comparison of the antiepileptogenic efficacy of 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