	Animal					Human
Tissues, structures, and nuclei	Alcohol exposure pattern and timing	Equivalent of human gestation	Structural or functional alterations	Behavioral disorders diagnosed later in life	Authors	Exposure timing	Age (years)	Structural or functional alterations	Behavioral disorders diagnosed later in life	Authors
Axogenesis	Ethanol exposure during the last week of fetal life; during the first postnatal week in rats	Second and third trimesters	Thinner thalamic- recipient zone of sensorimotor cortex; aberrant thalamo-cortical terminations in layer Va; disruption of cortico-cortical associative projections	Dysfunction of thalamo-cortical relationships and altered information integration	Minciacchi et al. 1993 [99] ; Granato et al. 2003 [145]	_	_	_	_	_
Dendrogenesis	Postnatal binge-like alcohol exposure on PD 4-9 in rats	Third trimester	Altered basilar dendritic complexity of layer II/III neurons in the medial PFC; decrease in both length and number of intersections connected to the neuronal soma.	Inefficient innervations of the soma and basilar dendrites by thalamic projections and thereby reducing performance on prefrontal- dependant behavioral tasks	He et al. 2005 [149] ; Hamilton et al. 2010 [141]	_	_	_	_	_
	Postnatal binge-like alcohol exposure on PD 4-9 in rats	Third trimester	Decreased spine density in layer II/III neurons of medial PFC; Reduced dendrite number of nodes and endings	Functional deficits in this cortical area	He et al. 2005 [149] ; Whitcher and Klintsova 2008 [142]	_	_	_	_	_
	Chronic alcohol exposure from pregestational stage until weaning in rats	First, second and third trimesters	Higher proportion of stubby or wide spines, but decreased percentage of thin spines	Thin spines may propagate the synaptic potentials more efficiently than stubby or wide spines, causing altered electrical excitability	Tarelo-Acuña et al. 2000 [139]	_	_	_	_	_
Interneurons	Binge-type ethanol exposure on GD13-GD16 in mice, rat model of fetal alcohol spectrum disorder	Second and third trimesters	Aberrant migration and loss of GABAergic interneurons, indelible abnormal cortical and hippocampal circuits, disturbances of GABA/glutamate ratios in medial prefrontal cortex (mPFC)	Synaptic excitatory- inhibitory imbalance causing attention- deficit/hyperactivity disorders	Skorput et al., 2015 [175] ; Delatour et al. 2020 [55] ; Tang et al. 2019 [40]	_	_	_	_	_
Synaptogenesis and synaptic plasticity	Binge-type ethanol exposure on GD13.5-GD16.5 and P7 in mice	Second and third trimesters	Delayed synaptogenesis, Impaired synaptic connectivity and plasticity	Impaired fear conditioning, reduced memory performance	Lovinger and Abrahao, 2018 [156] ; Bird et al. 2020 [159] ; Almeida et al. 2020 [54]	Adolescent alcohol exposure	_	Altered synaptic remode-ling and neurogenesis in key brain regions	Anxiety, high levels of emotion and impulsive behavior, arresting the development of executive function	Kyzar et al. 2016 [155]
Myelinogenesis	Maternal binge-like alcohol consumption in during gestation and lactation in mice	Second and third trimesters	Oligodendrocyte precursor cells apoptosis and altered differentiation, myelin damage in both prefrontal cortex and hippocampus; white matter injury	Impaired cognitive functions and motor coordination	Newville et al. 2017 [190] ; Cantacorps et al., 2017 [188]	Prenatal alcohol exposure	10 years 12.2 - 21.4 weeks gestation	Poorer myelination in cerebellar peduncles Dysmyelination, Disruption of white matter integrity	Visual-motor Deficits Changes in executive function	Fan et al., 2015 [198] ; Sowell et al. 2008 [199] ; Gautam et al. 2014 [200] ; Darbinian et al. 2021 [201]
White matter	Binge model of early prenatal alcohol exposure in sheep; and posnatal in mouse	First trimester and third trimesters	Lesions in the temporal, parietal, and occipital white matte; white matter atrophy in the corpus callosum and mPFC	Cognitive impairment; Long-lasting effects on neurobehavioral functions	Watari et al 2006 [210] ; Rice and Gu 2019 [28]	In utero exposure to alcohol	Shortly after birth; age range 6 - 17	White matter atrophy, particularly in frontal lobes; Brain white matter microstructure damaged	Persistent impaired cognitive and executive functions	Gautam et al. 2014 [200] ; Darbinian and Selzer 2022 [187]