Prevention of alcohol-induced learning deficits in fetal alcohol syndrome mediated through NMDA and GABA receptors

Laura Toso, Sarah H. Poggi, Robin Roberson, Jade Woodard, Jane Park, Daniel Abebe, Catherine Y. Spong

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Objective: Vasoactive intestinal peptide (VIP)-related peptides prevented the learning deficit in the offspring in a model for fetal alcohol syndrome. We evaluated whether the mechanism of the peptide protection included NR2B, NR2A, and GABAAα5. Study design: Timed, pregnant C57BL6/J mice were injected on gestational day 8 with alcohol (0.03 mL/kg), placebo, or alcohol plus peptides. Embryos were harvested after 6 hours, 24 hours, and on gestational day 18. Some of the litters were allowed to deliver, and the adult brains harvested after the offspring were tested for learning. Calibrator-normalized relative real-time polymerase chain reaction (PCR) was performed using primers for NR2B, NR2A, and GABAAα5 with GAPDH standardization. Statistic: analysis of variance (ANOVA) and Fisher PLSD, P < .05 was considered significant. Results: In the embryo, the peptides prevented NR2B rise (P < .001) at 6 hours, NR2B down-regulation (P = .002), and GABAAα5 decrease (P < .01) on gestational day 18. In the adult, the peptides prevented NR2B down-regulation (P = .01) and NR2A up-regulation (P < .001). Conclusion: VIP-related peptides prevented alcohol-induced changes in NR2B, NR2A, and GABAAα 5. This may explain, at least in part, the peptides' prevention of alcohol-induced learning deficits.

Original languageEnglish (US)
Pages (from-to)681-686
Number of pages6
JournalAmerican journal of obstetrics and gynecology
Volume194
Issue number3
DOIs
StatePublished - Mar 1 2006
Externally publishedYes

Keywords

  • Alcohol
  • Fetal alcohol syndrome
  • GABA
  • Learning
  • NMDA
  • Neurotrophic factors

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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