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The PreEE\u2010induced abnormal tangential migration involves, in part, ethanol potentiating GABA\n                      <jats:sub>A<\/jats:sub>\n                      receptor\u2010mediated depolarization, the latter due to elevated intracellular chloride sustained primarily by the Na\u2010K\u2010Cl cotransporter NKCC1 in embryonic GINs. We previously reported that coincident administration of the NKCC1 antagonist bumetanide with PreEE prevents the PreEE\u2010induced aberrant migration of GINs in the mPFC. However, such simultaneous dispensing rarely occurs in real life. In this light, the present study assessed whether bumetanide administered after PreEE mitigates the PreEE\u2010induced aberrant tangential migration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>NKCC1\u2010like immunofluorescence was assessed following immunohistochemical processing of 30\u2010\u03bcm cryosections derived from embryonic day (E)14.5 wild\u2010type mouse brains. Nkx2.1Cre\u2010Ai14 mice were used to genetically label MGE\u2010derived GINs. Pregnant dams were fed 5% ethanol (w\/w) from E13.5 to E16.5, followed by bumetanide treatment (320\u2009mg\/kg liquid diet) from E17.5 until postnatal day (P) 0 (birth). Forty\u2010micron cryosections from brains of progeny were collected at P0, and the density as well as spatial distribution of tdTomato\u2010fluorescent (Nkx2.1+) GINs in the mPFC quantified.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Within the timeframe of PreEE, the NKCC1 protein is expressed ubiquitously in the embryonic mouse brain, including the dorsomedial telencephalon, the precursor to mPFC. PreEE increased the overall density of Nkx2.1+ GINs and accelerated their dorsal\u2010to\u2010ventral dispersion across the developing mPFC. Post\u2010PreEE treatment with the NKCC1 antagonist bumetanide diminished these effects, reducing dorsal accumulation while preserving the baseline population of GINs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These results indicate that blocking the NKCC1 chloride importer bumetanide can mitigate PreEE\u2010induced interneuronopathy when administered after PreEE, implicating NKCC1 as a potential pharmacological target for post\u2010PreEE therapeutic intervention of FASD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.70375","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T04:39:47Z","timestamp":1784090387000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The\n                    <scp>NKCC1<\/scp>\n                    Antagonist Bumetanide, Administered After Prenatal Alcohol Exposure, Mitigates Ethanol\u2010Induced Aberrance in Tangential Migration of\n                    <scp>GABAergic<\/scp>\n                    Interneurons in Mouse Medial Prefrontal Cortex"],"prefix":"10.1111","volume":"50","author":[{"given":"Betul","family":"Koc","sequence":"first","affiliation":[{"name":"Department of Molecular and Systems Biology Geisel School of Medicine at Dartmouth  Hanover New Hampshire USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander G. 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