title: Prenatal ethanol (EtOH) exposure alters the sensitivity of the adult dentate gyrus to acute EtOH exposure.
abstract: BACKGROUND
  Prenatal ethanol (EtOH) exposure results in a spectrum of structural, cognitive, and behavioral abnormalities, collectively termed "fetal alcohol spectrum disorders" (FASDs). The hippocampal formation, an area of the brain strongly linked with learning and memory, is particularly vulnerable to the teratogenic effects of EtOH. Prenatal EtOH exposure can lead to long-lasting impairments in the ability to process spatial information, as well as produce long-lasting deficits in the ability of animals to exhibit long-term potentiation (LTP), a biological model of learning and memory processing. These deficits also have the ability to facilitate EtOH and/or other drug abuse later in life. This study sought to determine prenatal EtOH exposure altered the effects of acute EtOH application on synaptic plasticity.
  
  
  METHODS
  Prenatal EtOH exposure was modeled using a liquid diet where dams were given 1 of 3 diets: (i) a liquid diet containing EtOH (35.5% EtOH-derived calories), (ii) a liquid diet, isocaloric to the EtOH diet, but with maltose-dextrin substituting for the EtOH-derived calories, and (iii) an ad libitum diet of standard rat chow. Extracellular recordings from transverse brain slices (350 μm) prepared from 50- to 70-day-old rats, following prenatal EtOH exposure (gestational day 1 to 21). LTP was examined in the dentate gyrus following acute EtOH exposure (0, 20, or 50 mM) in these slices.
  
  
  RESULTS
  Prenatal EtOH exposure attenuated LTP in the adult dentate gyrus. In control offspring, acute application of EtOH in adulthood attenuated (20 mM) or blocked (50 mM) LTP. Conversely, the effect of acute EtOH application on LTP was not as pronounced in prenatal EtOH offspring.
  
  
  CONCLUSIONS
  Prenatal EtOH exposure alters the sensitivity of the adult dentate gyrus to acute EtOH application producing a long-lasting tolerance to the inhibitory effects of EtOH. This decreased sensitivity may provide a mechanism promoting the formation of drug-associated memories and help explain the increased likelihood of developing an alcohol dependency often observed in individuals with FASDs.
authors.affiliation: Division of Medical Sciences, University of Victoria, Victoria, British Columbia, Canada; Department of Biology, University of Victoria, Victoria, British Columbia, Canada.
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Helfer
authors.forename: Emily R
authors.initials: ER
authors.lastname: White
authors.forename: Brian R
authors.initials: BR
authors.lastname: Christie
mesh_terms: D000367:Age Factors; D000818:Animals; D018891:Dentate Gyrus / Q000187:drug effects* / Q000502:physiology*; D000431:Ethanol / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology; D008297:Male; D009924:Organ Culture Techniques; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000431:Ethanol
keywords: Acute Ethanol; Fetal Alcohol Spectrum Disorders; Hippocampal Formation; Long-Term Potentiation; Synaptic Plasticity