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Related Experiment Video

Updated: May 12, 2026

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

DNA methylation program in developing hippocampus and its alteration by alcohol.

Yuanyuan Chen¹, Nail Can Ozturk, Feng C Zhou

¹Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.

|April 2, 2013

Summary

Fetal alcohol exposure disrupts the DNA methylation program crucial for hippocampal development. This disruption impacts neuronal differentiation and maturation, potentially explaining learning deficits in Fetal Alcohol Spectrum Disorders (FASD).

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Last Updated: May 12, 2026

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

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Published on: August 5, 2017

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Optimized Analysis of DNA Methylation and Gene Expression from Small, Anatomically-defined Areas of the Brain

Optimized Analysis of DNA Methylation and Gene Expression from Small, Anatomically-defined Areas of the Brain

Published on: July 12, 2012

Area of Science:

Neuroscience
Developmental Biology
Epigenetics

Background:

Hippocampal development involves independent neurogenesis, migration, and maturation of Cornus Ammonis (CA) and dentate gyrus (DG) regions.
This developmental stage is susceptible to environmental stressors, with unclear underlying mechanisms.
Alcohol exposure affects genes regulating neuronal development, potentially contributing to Fetal Alcohol Spectrum Disorders (FASD)-related cognitive deficits.

Purpose of the Study:

To investigate the role of the DNA methylation program (DMP) in hippocampal neuronal differentiation and maturation.
To determine how fetal alcohol exposure impacts this DMP during critical developmental periods.

Main Methods:

C57BL/6 mice were exposed to ethanol via liquid diet from gestation day 7 to 16.
Control groups included pair-fed and chow-fed mice.
Analysis focused on DNA methylation marks (5-methylcytidine, 5-hydroxylmethylcytidine) and associated proteins in the hippocampus.

Main Results:

A characteristic DMP, including 5-methylcytidine (5mC) and 5-hydroxylmethylcytidine (5hmC), spatiotemporally guided hippocampal neuronal differentiation and maturation.
Alcohol exposure impaired the acquisition and progression of these methylation marks.
Alcohol altered the nuclear chromatin translocation of methylation marks, correlating with developmental retardation.

Conclusions:

The DNA methylation program is integral to hippocampal neuronal differentiation and maturation.
Fetal alcohol exposure disrupts this epigenetic programming, potentially underlying developmental deficits.
Understanding these mechanisms is crucial for addressing the neurodevelopmental consequences of FASD.