{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T06:05:56Z","timestamp":1792735556155,"version":"4.5.0"},"reference-count":55,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2011,9,20]],"date-time":"2011-09-20T00:00:00Z","timestamp":1316476800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2012,3]]},"abstract":"<jats:p>\n                    <jats:bold>Background:\u2002<\/jats:bold>\n                    It has been estimated that approximately 12% of women consume alcohol at some time during their pregnancy, and as many as 5% of children born in the United States are impacted by prenatal alcohol exposure (PAE). The range of physical, behavioral, emotional, and social dysfunctions that are associated with PAE are collectively termed fetal alcohol spectrum disorder (FASD).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:\u2002<\/jats:bold>\n                    Using a saccharin\u2010sweetened ethanol solution, we developed a limited access model of PAE. C57BL\/6J mice were provided access to a solution of either 10% (w\/v) ethanol and 0.066% (w\/v) saccharin or 0.066% (w\/v) saccharin (control) for 4\u2003h\/d. After establishing consistent drinking, mice were mated and continued drinking during gestation. Following parturition, solutions were decreased to 0% in a stepwise fashion over a period of 6\u2003days. Characterization of the model included measurements of maternal consumption patterns, blood ethanol levels, litter size, pup weight, maternal care, and the effects of PAE on fear\u2010conditioned and spatial learning, and locomotor activity.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:\u2002<\/jats:bold>\n                    Mothers had mean daily ethanol intake of 7.17\u2003\u00b1\u20030.17\u2003g ethanol\/kg body weight per day, with average blood ethanol concentrations of 68.5\u2003\u00b1\u20039.2\u2003mg\/dl after 2\u2003hours of drinking and 88.3\u2003\u00b1\u200311.5\u2003mg\/dl after 4\u2003hours of drinking. Food and water consumption, maternal weight gain, litter size, pup weight, pup retrieval times, and time on nest did not differ between the alcohol\u2010exposed and control animals. Compared with control offspring, mice that were exposed to ethanol prenatally displayed no difference in spontaneous locomotor activity but demonstrated learning deficits in 3 hippocampal\u2010dependent tasks: delay fear conditioning, trace fear conditioning, and the delay nonmatch to place radial\u2010arm maze task.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions:\u2002<\/jats:bold>\n                    These results indicate that this model appropriately mimics the human condition of PAE and will be a useful tool in studying the learning deficits seen in FASD.\n                  <\/jats:p>","DOI":"10.1111\/j.1530-0277.2011.01644.x","type":"journal-article","created":{"date-parts":[[2011,9,20]],"date-time":"2011-09-20T17:50:14Z","timestamp":1316541014000},"page":"457-466","source":"Crossref","is-referenced-by-count":124,"title":["A Limited Access Mouse Model of Prenatal Alcohol Exposure that Produces Long\u2010Lasting Deficits in 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