{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T15:33:01Z","timestamp":1759073581944,"version":"3.41.2"},"reference-count":32,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,3,21]],"date-time":"2017-03-21T00:00:00Z","timestamp":1490054400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Randolph-Macon College Chenery and Craigie Grants"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Prenatal alcohol exposure can result in neurological changes in affected individuals and may result in the emergence of a broad spectrum of neurobehavioral abnormalities termed fetal alcohol spectrum disorders (<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>). The effects of ethanol exposure during development are both time and dose dependent. Although many animal models of<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>use more chronic ethanol exposure, acute developmental alcohol exposure may also cause long\u2010lasting neuronal changes. Our research employed behavioral measures to assess the effects of a single early postnatal ethanol intoxication event in mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>Mice were dosed at postnatal day 6 (a 2.5\u00a0g\/kg dose of ethanol or a saline control administered twice, 2\u00a0hr apart) as a model of third trimester binge drinking in humans. This exposure was followed by behavioral assessment in male mice at 1\u00a0month (1M) and at 4\u00a0months of age (4M), using the Barnes maze (for learning\/memory retrieval), exploratory behavior, and a social responsiveness task.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Ethanol\u2010exposed mice appeared to be less motivated to complete the Barnes maze at 1M, but were able to successfully learn the maze. However, deficits in long\u2010term spatial memory retrieval were observed in ethanol\u2010exposed mice when the Barnes maze recall was measured at 4M. No significant differences were found in open field behavior or social responsiveness at 1M or 4M of age.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Acute ethanol exposure at P6 in mice leads to mild but long\u2010lasting deficits in long\u2010term spatial memory. Results suggest that even brief acute exposure to high ethanol levels during the third trimester equivalent of human pregnancy may have a permanent negative impact on the neurological functioning of the offspring.<\/jats:p><\/jats:sec>","DOI":"10.1002\/brb3.636","type":"journal-article","created":{"date-parts":[[2017,3,22]],"date-time":"2017-03-22T15:46:54Z","timestamp":1490197614000},"source":"Crossref","is-referenced-by-count":16,"title":["Acute ethanol exposure during late mouse neurodevelopment results in long\u2010term deficits in memory retrieval, but not in social responsiveness"],"prefix":"10.1002","volume":"7","author":[{"given":"Katherine","family":"Houl\u00e9","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine Medical College of South Carolina Charleston SC USA"},{"name":"Department of Biology Randolph\u2010Macon College Ashland VA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Myshake","family":"Abdi","sequence":"additional","affiliation":[{"name":"Department of Biology Hampden\u2010Sydney College Farmville VA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4295-2272","authenticated-orcid":false,"given":"Erin B. 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