Alterations in phosphorylated cyclic adenosine monophosphate response element of binding protein activity: a pathway for fetal alcohol syndrome-related neurotoxicity - 12/08/11
, Irene Cameroni, MD b, Laura Toso, MD a, Daniel Abebe, MS a, Stephanie Bissel, BS a, Catherine Y. Spong, MD a
Reprints: Robin Roberson, BA, Unit on Perinatal and Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20895Résumé |
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.
Le texte complet de cet article est disponible en PDF.Key words : apoptosis, fetal alcohol syndrome, hippocampus, mouse, phosphorylated cyclic adenosine monophosphate response element of binding protein
Plan
| Cite this article as: Roberson R, Cameroni I, Toso L, et al. Alterations in phosphorylated cyclic adenosine monophosphate response element of binding protein activity: a pathway for fetal alcohol syndrome-related neurotoxicity. Am J Obstet Gynecol 2009;200:193.e1-193.e5. |
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| This study was supported in part by the Division of Intramural Research, National Institute of Child Health and Human Development, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health. |
Vol 200 - N° 2
P. 193.e1-193.e5 - février 2009 Retour au numéro
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