{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:24:39Z","timestamp":1791300279655,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,2,26]],"date-time":"2013-02-26T00:00:00Z","timestamp":1361836800000},"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; Exp Res"],"published-print":{"date-parts":[[2013,6]]},"abstract":"Background<\/jats:title>Fetal alcohol syndrome and related disorders (commonly referred to as fetal alcohol spectrum disorder, or FASD<\/jats:styled-content>) cause significant hardships to the individuals affected. Previously, histological studies in animals have characterized developmental cerebral cortical abnormalities that result from prenatal ethanol (E<\/jats:styled-content>tOH<\/jats:styled-content>) exposure. Additionally, magnetic resonance imaging (MRI<\/jats:styled-content>) studies have identified abnormalities associated with fetal E<\/jats:styled-content>tOH<\/jats:styled-content> exposure in the cerebral cortices of human children and adolescents. However, there is still a need to bridge the gap between human MRI<\/jats:styled-content> studies and animal histological studies. The goal of the research presented here was to perform postmortem MRI<\/jats:styled-content> experiments on rodents, during time periods relative to late human gestation through adulthood, to characterize anomalies associated with FASD<\/jats:styled-content> throughout development. Additionally, by determining how histologically identified abnormalities are manifest in MRI<\/jats:styled-content> measurements specifically during the critical early time points, neuroimaging\u2010based biomarkers of FASD<\/jats:styled-content> can potentially be identified at much earlier ages in humans, thus reducing the impact of these disorders.<\/jats:p><\/jats:sec>Methods<\/jats:title>Cerebral cortical volume, thickness, and surface area were characterized by ex vivo MRI<\/jats:styled-content> in Long\u2010Evans rat pups born from dams that were E<\/jats:styled-content>tOH<\/jats:styled-content>\u2010treated, maltose\/dextrin\u2010treated, or untreated throughout gestation at 6 developmental time points (postnatal day [P<\/jats:styled-content>] 0, P<\/jats:styled-content>3, P<\/jats:styled-content>6, P<\/jats:styled-content>11, P<\/jats:styled-content>19, and P<\/jats:styled-content>60).<\/jats:p><\/jats:sec>Results<\/jats:title>Brain volume, isocortical volume, isocortical thickness, and isocortical surface area were all demonstrated to be reduced following prenatal exposure to E<\/jats:styled-content>tOH<\/jats:styled-content>. Significant differences among the treatment groups were observed throughout the range of time points studied, allowing for a comprehensive view of FASD<\/jats:styled-content> influenced MRI<\/jats:styled-content> outcomes throughout development. Isocortical surface area and isocortical thickness results contributed independent information important to interpreting effects of prenatal E<\/jats:styled-content>tOH<\/jats:styled-content> exposure on cerebral cortical development. Additionally, regional patterns in cortical thickness differences suggested primary sensory areas were particularly vulnerable to gestational E<\/jats:styled-content>tOH<\/jats:styled-content> exposure.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Structural MRI<\/jats:styled-content> measurements were in accordance with previous histological studies performed in animal models of FASD<\/jats:styled-content>. In addition to establishing a summary of MRI<\/jats:styled-content> outcomes throughout development in FASD<\/jats:styled-content>, this research suggests that MRI<\/jats:styled-content> techniques are sufficiently sensitive to detect neuroanatomical effects of fetal E<\/jats:styled-content>tOH<\/jats:styled-content> exposure on development of the cerebral cortex during the period of time corresponding to late gestation in humans. Importantly, this research provides a link between animal histological data and human MRI<\/jats:styled-content> data.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12051","type":"journal-article","created":{"date-parts":[[2013,2,26]],"date-time":"2013-02-26T19:56:53Z","timestamp":1361908613000},"page":"924-932","source":"Crossref","is-referenced-by-count":38,"title":["The Influence of Fetal Ethanol Exposure on Subsequent Development of the Cerebral Cortex as Revealed by Magnetic Resonance Imaging"],"prefix":"10.1111","volume":"37","author":[{"given":"Lindsey A.","family":"Leigland","sequence":"first","affiliation":[{"name":"Advanced Imaging Research Center Oregon Health & Science University Portland Oregon"},{"name":"Department of Behavioral Neuroscience Oregon Health & Science University Portland Oregon"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew M.","family":"Ford","sequence":"additional","affiliation":[{"name":"Department of Behavioral Neuroscience Oregon 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