title: The Impact of Prenatal Ethanol Exposure on Neuroanatomical and Behavioral Development in Mice.
abstract: BACKGROUND
  In utero alcohol, or ethanol (EtOH), exposure produces developmental abnormalities in the brain of the fetus, which can result in lifelong behavioral abnormalities. Fetal alcohol spectrum disorders (FASD) is a term used to describe a range of adverse developmental conditions caused by EtOH exposure during gestation. Children diagnosed with FASD potentially exhibit a host of phenotypes including growth retardation, facial dysmorphology, central nervous system anomalies, abnormal behavior, and cognitive deficits. Previous research suggests that abnormal gene expression and circuitry in the neocortex may underlie reported disabilities of learning, memory, and behavior resulting from early exposure to alcohol (J Neurosci, 33, 2013, 18893).
  
  
  METHODS
  Here, we utilize a mouse model of FASD to examine effects of prenatal EtOH exposure (PrEE), on brain anatomy in newborn (postnatal day [P]0), weanling (P20), and early adult (P50) mice. We correlate abnormal cortical and subcortical anatomy with atypical behavior in adult P50 PrEE mice. In this model, experimental dams self-administered a 25% EtOH solution throughout gestation (gestational days 0 to 19, day of birth), generating the exposure to the offspring.
  
  
  RESULTS
  Results from these experiments reveal long-term alterations to cortical anatomy, including atypical developmental cortical thinning, and abnormal subcortical development as a result of in utero EtOH exposure. Furthermore, offspring exposed to EtOH during the prenatal period performed poorly on behavioral tasks measuring sensorimotor integration and anxiety.
  
  
  CONCLUSIONS
  Insight from this study will help provide new information on developmental trajectories of PrEE and the biological etiologies of abnormal behavior in people diagnosed with FASD.
authors.affiliation: Interdepartmental Graduate Program in Neuroscience, University of California, Riverside, Riverside, California.
authors.forename: Charles W
authors.initials: CW
authors.lastname: Abbott
authors.affiliation: Department of Psychology, University of California, Riverside, Riverside, California.
authors.forename: Olga O
authors.initials: OO
authors.lastname: Kozanian
authors.affiliation: Department of Psychology, University of California, Riverside, Riverside, California.
authors.forename: Joseph
authors.initials: J
authors.lastname: Kanaan
authors.affiliation: Department of Psychology, University of California, Riverside, Riverside, California.
authors.forename: Kara M
authors.initials: KM
authors.lastname: Wendel
authors.affiliation: Interdepartmental Graduate Program in Neuroscience, University of California, Riverside, Riverside, California.|Department of Psychology, University of California, Riverside, Riverside, California.
authors.forename: Kelly J
authors.initials: KJ
authors.lastname: Huffman
mesh_terms: D000818:Animals; D001007:Anxiety; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000002:abnormalities / Q000187:drug effects* / Q000196:embryology; D002452:Cell Count; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000002:abnormalities / Q000187:drug effects / Q000196:embryology; D004195:Disease Models, Animal; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders; D051379:Mice; D009929:Organ Size; D004856:Postural Balance / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
chemical_list: D002492:Central Nervous System Depressants; D000431:Ethanol
keywords: Anatomy; Brain Development; Fetal Alcohol Spectrum Disorders; Neocortex; Prenatal Alcohol Exposure