Alterations in phosphorylated cyclic adenosine monophosphate response element of binding protein activity: a pathway for fetal alcohol syndrome-related neurotoxicity

Robin Roberson, Irene Cameroni, Laura Toso, Daniel Abebe, Stephanie Bissel, Catherine Y. Spong

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Objective: Fetal alcohol syndrome (FAS) is the leading cause of a spectrum of preventable nongenetic learning and behavioral disorders. In adult (FAS) mice, we measured phosphorylated cyclic adenosine monophosphate response element of binding protein (pCREB) staining in hippocampal subregions to evaluate a possible mechanism underlying FAS learning deficits. Study Design: Pregnant C57BL6/J mice were treated on gestational day 8 with alcohol or control (saline). After learning assessment, the offspring were perfused for immunohistochemistry and brain sections probed using SER 133 pCREB antibody. Relative staining density was assessed using National Institutes of Health Image software. Statistical analysis included analysis of variance with P < .05 considered significant. Results: In all hippocampal subregions, pCREB staining was greater in the control animals than in the alcohol-treated group (P ≤ .0001). Conclusion: In utero alcohol exposure decreased pCREB activity in hippocampal subregions of adult mice. The dentate gyrus had the most robust cumulative decrease in pCREB staining, suggesting FAS adult learning deficits may correlate to enhanced dentate gyrus neurodegeneration.

Original languageEnglish (US)
Pages (from-to)193.e1-193.e5
JournalAmerican journal of obstetrics and gynecology
Volume200
Issue number2
DOIs
StatePublished - Feb 2008
Externally publishedYes

Keywords

  • apoptosis
  • fetal alcohol syndrome
  • hippocampus
  • mouse
  • phosphorylated cyclic adenosine monophosphate response element of binding protein

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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