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The use of phenobarbital continues despite growing evidence that it exerts suboptimal seizure control and is associated with long\u2010term alterations in brain structure, function, and behavior. Alterations following neonatal phenobarbital exposure include acute induction of neuronal apoptosis, disruption of synaptic development in the striatum, and a host of behavioral deficits. These behavioral deficits include those in learning and memory mediated by the hippocampus. However, the synaptic changes caused by acute exposure to phenobarbital that lead to lasting effects on brain function and behavior remain understudied.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Postnatal day (P)7 rat pups were treated with phenobarbital (75\u00a0mg\/kg) or saline. On P13\u201014 or P29\u201037, acute slices were prepared and whole\u2010cell patch\u2010clamp recordings were made from <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>1 pyramidal neurons.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At P14 we found an increase in miniature inhibitory postsynaptic current (<jats:styled-content style=\"fixed-case\">mIPSC<\/jats:styled-content>) frequency in the phenobarbital\u2010exposed as compared to the saline\u2010exposed group. In addition to this change in <jats:styled-content style=\"fixed-case\">mIPSC<\/jats:styled-content> frequency, the phenobarbital group displayed larger bicuculline\u2010sensitive tonic currents, decreased capacitance and membrane time constant, and a surprising persistence of giant depolarizing potentials. At P29+, the frequency of <jats:styled-content style=\"fixed-case\">mIPSC<\/jats:styled-content>s in the saline\u2010exposed group had increased significantly from the frequency at P14, typical of normal synaptic development; at this age the phenobarbital\u2010exposed group displayed a lower <jats:styled-content style=\"fixed-case\">mIPSC<\/jats:styled-content> frequency than did the control group. Spontaneous inhibitory postsynaptic current (sIPSC) frequency was unaffected at either P14 or P29+.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>These neurophysiological alterations following phenobarbital exposure provide a potential mechanism by which acute phenobarbital exposure can have a long\u2010lasting impact on brain development and behavior.<\/jats:p><\/jats:sec>","DOI":"10.1111\/epi.13990","type":"journal-article","created":{"date-parts":[[2018,1,10]],"date-time":"2018-01-10T03:10:32Z","timestamp":1515553832000},"page":"333-344","source":"Crossref","is-referenced-by-count":36,"title":["Neonatal phenobarbital exposure disrupts <scp>GABA<\/scp>ergic synaptic maturation in rat <scp>CA<\/scp>1 neurons"],"prefix":"10.1111","volume":"59","author":[{"given":"Nour","family":"Al\u2010Muhtasib","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Physiology Georgetown University Washington DC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6479-8635","authenticated-orcid":false,"given":"Alberto","family":"Sepulveda\u2010Rodriguez","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Physiology Georgetown University Washington DC USA"},{"name":"Interdisciplinary Program in Neuroscience Georgetown University Washington DC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefano","family":"Vicini","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Physiology Georgetown University Washington DC USA"},{"name":"Interdisciplinary Program in Neuroscience Georgetown University Washington DC USA"},{"name":"Department of Neuroscience Georgetown University Washington DC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1763-060X","authenticated-orcid":false,"given":"Patrick A.","family":"Forcelli","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Physiology Georgetown University Washington DC USA"},{"name":"Interdisciplinary Program in Neuroscience Georgetown University Washington DC USA"},{"name":"Department of Neuroscience Georgetown University Washington DC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2018,1,5]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pediatrneurol.2011.11.006"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199908123410704"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199002083220604"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0378-3782(79)90022-7"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.222550499"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/epi.13335"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2011.03297.x"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/epi.13365"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.287.5455.1056"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-03-00876.2003"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.23600"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2010.02603.x"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2012.02.001"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.111.188862"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yebeh.2016.01.018"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yebeh.2014.07.010"},{"key":"e_1_2_8_18_1","first-page":"101","article-title":"Consequences of early postnatal benzodiazepines exposure in rats. 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