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We also investigated the ability of bumetanide to restore the efficacy of diazepam following\n                      <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Kainic acid (\n                      <jats:styled-content style=\"fixed-case\">KA<\/jats:styled-content>\n                      )\u2013induced\n                      <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>\n                      in vivo and 0\u2010Mg\n                      <jats:sup>2+<\/jats:sup>\n                      \u2010induced seizure\u2010like events (\n                      <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>\n                      s) in vitro were monitored using electroencephalography (\n                      <jats:styled-content style=\"fixed-case\">EEG<\/jats:styled-content>\n                      ) recordings in freely moving adult male mice and extracellular field potential recordings in acute entorhinal cortex\u2010hippocampus slices, respectively. The ability of bumetanide to decrease epileptiform activity and prevent the development of pharmacoresistance to diazepam following\n                      <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>\n                      was evaluated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Bumetanide treatment significantly reduced\n                      <jats:styled-content style=\"fixed-case\">KA<\/jats:styled-content>\n                      \u2010induced ictal activity in vivo and\n                      <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>\n                      s in vitro. In addition, bumetanide restored the efficacy of diazepam in decreasing ictal activity following\n                      <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>\n                      in both the in vivo and in vitro models.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>\n                      Our data demonstrate an anticonvulsant effect of bumetanide on\n                      <jats:styled-content style=\"fixed-case\">KA<\/jats:styled-content>\n                      \u2010induced seizures in adult mice, suggesting a role for chloride plasticity in seizure progression. These data also demonstrate that the erosion of inhibition during seizure progression could underlie the development of pharmacoresistant\n                      <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>\n                      and implicate a role for chloride plasticity in this process.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/epi.13270","type":"journal-article","created":{"date-parts":[[2015,12,13]],"date-time":"2015-12-13T03:37:11Z","timestamp":1449977831000},"page":"222-232","source":"Crossref","is-referenced-by-count":76,"title":["Bumetanide reduces seizure progression and the development of pharmacoresistant status epilepticus"],"prefix":"10.1111","volume":"57","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8586-0469","authenticated-orcid":false,"given":"Sudhir","family":"Sivakumaran","sequence":"first","affiliation":[{"name":"Department of Biosciences University of Helsinki Helsinki 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