Nina Kaminen-Ahola
Group Leader

Department of Medical

P.O. Box 63
(Haartmaninkatu 8)
00014 University of Helsinki


+358 (0)50 4482768

Mouse model for alcohol exposure during early pregnancy

Prenatal alcohol exposure may cause a wide spectrum of disorders such as learning difficulties and congenital deformations to the child. The mechanisms by which alcohol affects fetal development remain unknown, and the defects caused to the child are difficult to diagnose.

FAS mouse model

Mouse models in which the dam ingests alcohol during early pregnancy have been observed to exhibit symptoms similar to human fetal alcohol syndrome (FAS): retardation of growth, structural abnormalities in corresponding parts of the face and skull, as well as hyperactivity. Such early exposure begins at fertilisation and continues to the start of the development of the nervous system. In humans, this corresponds developmentally with three or four weeks after fertilisation (weeks 3‒6 of the clinical pregnancy). At this time the expectant mother is often unaware of her pregnancy.

Changes in the epigenome and gene function

Early pregnancy is a period of active cell division and differentiation. An individual epigenome that regulates gene function is formed for each cell type containing a similar DNA strand. Studies of animal models have indicated that this stage of development is sensitive to environmental effects. Early changes in the epigenome may spread widely to different tissues through cell division and differentiation.

We have already demonstrated by using the epigenetically sensitive Agouti viable yellow (Avy) allele that early alcohol exposure permanently alters the epigenome of the developing mouse offspring, gene transcription, and the appearance of the pup. Now our goal is to investigate whether alcohol ingestion during early pregnancy causes changes in the function of normal genes (other than the Avy allele) and whether this is due to changes to the epigenome. In addition, we want to know whether these changes manifest later in the gene function of the offspring and whether they cause symptoms typical of prenatal alcohol exposure in humans.

Read more about the mouse model:

Kaminen-Ahola N ja muut, 2010. Maternal Ethanol Consumption Alters the Epigenotype and the Phenotype of Offspring in a Mouse Model. PLoS Genetics 6(1) e1000811

Kaminen-Ahola N ja muut, 2010. Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome. Birth Defects Res A Clin Mol Teratol 88: 818-826.

Sanchez Vega MC ja muut, 2013. Early gestational exposure to moderate concentrations of ethanol alters adult behaviour in C57BL/6J mice. Behav Brain Res. 252: 326-333.

Marjonen ja muut, 2015. Early Maternal Alcohol Consumption Alters Hippocampal DNA Methylation, Gene Expression and Volume in Offspring in a Mouse Model. PLoS ONE. DOI: 10.1371/journal.pone.0124931

Alcohol exposure during early pregnancy alters the epigenome, gene function and structure of the hippocampus in mouse offspring

This study focused on the hippocampus, a structure in the brain essential to memory and learning. It is known to be sensitive to the effects of alcohol. In this study, early alcohol exposure altered the epigenome that regulates gene function and the function of several genes in the hippocampi of young mouse pups.     Read more...