title: Effects of Developmental Alcohol Exposure on Potentiation and Depression of Visual Cortex Responses.
abstract: BACKGROUND
  Neuronal plasticity deficits are thought to underlie abnormal neurodevelopment in fetal alcohol spectrum disorders and in animal models of this condition. Previously, we found that alcohol exposure during a period that is similar to the last months of gestation in humans disrupts ocular dominance plasticity (ODP), as measured in superficial cortical layers. We hypothesize that exposure to alcohol can differentially affect the potentiation and depression of responses that are necessary for activity-dependent sprouting and pruning of neuronal networks. ODP is an established paradigm that allows the assessment of activity-dependent depression and potentiation of responses in vivo.
  
  
  METHODS
  Mouse pups were exposed to 3.6 to 5 g/kg of ethanol in saline daily or every other day between postnatal days 4 and 9. Visual cortex plasticity was then assessed during the critical period for ODP using 2 techniques that separately record in layers 4 (visually evoked potentials [VEPs]) and 2/3 (optical imaging of intrinsic signals [OI]).
  
  
  RESULTS
  We discovered a layer-specific effect of early alcohol exposure. Recording of VEPs from layer 4 showed that while the potentiation component of ODP was disrupted in animals treated with alcohol when compared with saline controls, the depression component of ODP (Dc-ODP) was unaltered. In contrast, OI from layers 2/3 showed that Dc-ODP was markedly disrupted in alcohol-treated animals when compared with controls.
  
  
  CONCLUSIONS
  Combined with our previous work, these findings strongly suggest that developmental alcohol exposure has a distinct and layer-specific effect on the potentiation and depression of cortical responses after monocular deprivation.
authors.affiliation: Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia.|Department of Biology, University of Maryland, College Park, Maryland.
authors.forename: Crystal L
authors.initials: CL
authors.lastname: Lantz
authors.affiliation: Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York.
authors.forename: Grayson O
authors.initials: GO
authors.lastname: Sipe
authors.affiliation: Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York.
authors.forename: Elissa L
authors.initials: EL
authors.lastname: Wong
authors.affiliation: Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York.
authors.forename: Ania K
authors.initials: AK
authors.lastname: Majewska
authors.affiliation: Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia.|Department of Pediatrics, School of Medicine, University of Maryland, Baltimore, Maryland.
authors.forename: Alexandre E
authors.initials: AE
authors.lastname: Medina
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000431:Ethanol / Q000633:toxicity*; D005074:Evoked Potentials, Visual / Q000187:drug effects* / Q000502:physiology; D005260:Female; D008297:Male; D051379:Mice; D011247:Pregnancy; D012683:Sensory Deprivation / Q000502:physiology; D015349:Vision, Monocular / Q000187:drug effects* / Q000502:physiology; D014793:Visual Cortex / Q000187:drug effects* / Q000254:growth & development*
chemical_list: D000431:Ethanol
keywords: Fetal Alcohol Syndrome; Monocular Deprivation; Ocular Dominance; Visual Development; Visually Evoked Potentials