{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T06:29:24Z","timestamp":1785133764513,"version":"3.55.0"},"reference-count":14,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,1,7]],"date-time":"2013-01-07T00:00:00Z","timestamp":1357516800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Both early life inflammation and prolonged febrile seizures have been associated with increased excitation in the adult brain. We hypothesized this may be due in part to changes in the cation\u2010chloride cotransporter system. Rat pups received saline or lipopolysaccharide\/kainic acid (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">KA<\/jats:styled-content>) resulting in inflammation, followed by a behavioral febrile seizure (<jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content>) in approximately 50% of rats. Adult animals from the saline, inflammation, or inflammation\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content> groups underwent the following: (1) in vitro electrophysiologic studies; (2) Western blotting or polymerase chain reaction; or (3) application of the Na\u2010K\u2010Cl cotransporter 1 (<jats:styled-content style=\"fixed-case\">NKCC<\/jats:styled-content>1) blocker bumetanide to determine its effect on reversing increased excitability in vitro. The inflammation and inflammation\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content> groups demonstrated increased excitability in vitro and increased hippocampal protein expression of <jats:styled-content style=\"fixed-case\">NR2B<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">GABA<\/jats:styled-content><jats:sub>A<\/jats:sub> \u03b15 receptor subunits and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression of <jats:styled-content style=\"fixed-case\">NKCC<\/jats:styled-content>1. The inflammation\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content> group also had decreased protein expression of <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>luR2 and <jats:styled-content style=\"fixed-case\">GABA<\/jats:styled-content><jats:sub>A<\/jats:sub> \u03b11 receptor subunits and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein expression of <jats:styled-content style=\"fixed-case\">KCC<\/jats:styled-content>2. Bumetanide decreased in vitro 4\u2010aminopyridine\u2010induced inter\u2010ictal activity in the inflammation and inflammation\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content> groups. The results demonstrate early\u2010life inflammation with or without a behavioral <jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content> can lead to long\u2010lasting molecular changes and increased excitability in the adult rat hippocampus, although some changes are more extensive when inflammation is accompanied by behavioral seizure activity. Bumetanide is effective in reversing increased excitability in vitro, providing evidence for a causal role for cation\u2010chloride cotransporters and suggesting this drug may prove useful for treating epilepsy that develops after a <jats:styled-content style=\"fixed-case\">FS<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/epi.12061","type":"journal-article","created":{"date-parts":[[2013,1,7]],"date-time":"2013-01-07T14:17:06Z","timestamp":1357568226000},"source":"Crossref","is-referenced-by-count":45,"title":["Increased excitability and molecular changes in adult rats after a febrile seizure"],"prefix":"10.1111","volume":"54","author":[{"given":"Aylin Y.","family":"Reid","sequence":"first","affiliation":[{"name":"Hotchkiss Brain Institute University of Calgary Calgary Alberta Canada"},{"name":"Department of Clinical Neurosciences University of Calgary Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiarash","family":"Riazi","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute University of Calgary Calgary Alberta Canada"},{"name":"Department of Physiology and Pharmacology University of Calgary Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"Campbell Teskey","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute University of Calgary Calgary Alberta Canada"},{"name":"Department of Cell Biology and Anatomy University of Calgary Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quentin J.","family":"Pittman","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute University of Calgary Calgary Alberta Canada"},{"name":"Department of Physiology and Pharmacology University of Calgary Calgary Alberta Canada"},{"name":"Alberta Children's Hospital Research Institute University of Calgary Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,1,7]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20358"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awl018"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1901-08.2008"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2007.01.110"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2005.00294.x"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.0013-9580.2004.13704.x"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2005.00286.x"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2012.05.045"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2006.07.012"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3329-06.2006"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1017\/S0317167100008246"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0806682105"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2007.09.003"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4757-6376-8_10"}],"container-title":["Epilepsia"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1111%2Fepi.12061","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/epi.12061","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,15]],"date-time":"2023-10-15T05:43:53Z","timestamp":1697348633000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/epi.12061"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2013,1,7]]},"references-count":14,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2013,4]]}},"alternative-id":["10.1111\/epi.12061"],"URL":"https:\/\/doi.org\/10.1111\/epi.12061","archive":["Portico"],"relation":{},"ISSN":["0013-9580","1528-1167"],"issn-type":[{"value":"0013-9580","type":"print"},{"value":"1528-1167","type":"electronic"}],"subject":[],"published":{"date-parts":[[2013,1,7]]}}}