Cerebral cortex | Chronic alcohol exposure on GD 10 to 21 in rats, and throughout gestation in mice and rats | Second and third trimesters | Delayed pyramidal neurons migration and cortical stratification, thinning and Heterotopias in the cerebral cortex, altered development of the frontal lobe and impaired functional connectivity in the mPFC | Information integration and processing disorders, impaired executive functions | Miller 1993 [56] ; Fukui and Sakata-Haga 2009 [38] ; Tang et al. 2019 [40] | In utero alcohol exposure | Preadole- scent children with FASD | Smaller volume of grey matter, thinner cortex, reduced functional connectivity between cortical and deep grey matter structures | Impaired executive function with cognitive/ behavioral deficits | Donald et al., 2015 [26] ; Robertson et al. 2016 [52] ; Kingdon et al. 2016 [14] ; Rice and Gu 2019 [28] |
Lateral ventricule | Chronic alcohol exposure on GD 10 to 21 in rats; Binge-like exposure from GD12 to 15 | Second trimester | Dilation of the lateral ventricles, hypoplasia of the septum | Hydrocephalus | Sakata-Haga et al. 2004 [37] ; Sudheendran et al. 2013 [47] | Binge-like exposure during pregnancy | Gestational age: 5 - 12 weeks. | Abnormalities in the formation of the lateral ventricle walls; ventriculo-megaly | ? | Konovalov et al. (1997) [215] ; Lebel et al. (2011) [203] |
Corpus callosum | Binge model of early prenatal alcohol exposure in sheep | First trimester | Loosely bundled corpus callosum; enhanced corpus callosum and optic radiation white matter | Impaired information processing | Watari et al. 2006 [210] ; | Prenatal alcohol exposure | Under 5 years to adulthood | Alterations in the shape and volume of the corpus callosum, corpus callosum atrophy | Impaired executive function, visual and logical memories | Bookstein et al. 2002 [30] ; Donald et al. 2015 [26] ; |
Hypothalamic- pituitary adrenal axis | Binge-like prenatal ethanol exposure on GD7 in mice | Second trimester | Elevated corticosterone and adrenocorticotropic hormone (ACTH) levels | Increased anxiety-like behavior | Wieczorek et al. 2015 [214] | _ | _ | _ | _ | _ |
Hippocampus | Binge alcohol exposure on GD 10 to 21 in rats/on P1 throughout P8 in mice and rat | Second and third trimester | Aberrant distribution of mossy fibers, apoptosis, more cornered and ectopic pyramidal cells in the hippocampus in CA1, CA3 and GD | Defect of spatial memory | Bâ et al. 1999 [1] ; Sakata- Haga et al. 2003 [41] ; Smith et al. 2015 [76] | Binge-like drinking throughout pregnancy | Children with FASD | Small hippocampi; hippocampus more deformed at the head and tail | Cognitive deficits | Autti-Rämö et al. 2002 [23] ; Joseph et al., 2014 [180] ; Glass et al. 2014 [24] ; Cardenas et al. 2014 [25] |
Cerebellum | Chronic alcohol exposure on GD 10 to 21 in rats/ P4-9 in mice | Second and third trimester | Fusion of cerebellar folia and disruption of the cortical structure, losses of Purkinje and granule cells | Delayed motor development and ataxia | Sakata-Haga et al. 2001 [36] ; Fukui and Sakata-Haga 2009 [38] | Prenatal alcohol exposure | Children (13 years) | Smaller cerebellar volumes; hypoplastic cerebellar hemispheres | Impaired basic fine motor skills, attention deficits | Autti-Rämö et al. 2002 [23] ; Cardenas et al. 2014 [25] ; Donald et al., 2015 [26] . |
Brain weight | Binge-like alcohol exposure on postnatal day (PD) 4 trough 10 in rats | Third trimester | Reduced weight of the whole brain, forebrain, and cerebellum | Microencephaly and related disorders | Bonthius and West 1988 [32] | Binge-like drinking during first, second, and third trimesters | Infants | Reduced brain weight, reduced brain volume, reductions in frontal, temporal, parietal and occipital lobes. | Microencephaly and related disorders | Lebel et al. (2011) [203] ; Feldman et al., 2012 [204] . |