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Alcohol exposure decreases CREB binding protein expression and histone acetylation in the developing cerebellum

Weixiang Guo1, Erin L Crossey, Li Zhang

  • 1Department of Neurosciences, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States of America.

Plos One
|June 10, 2011
PubMed

Insights

Fetal alcohol exposure lowers CREB binding protein (CBP) levels in developing rat cerebellum. This reduction in CBP, crucial for gene expression, may cause motor deficits in fetal alcohol spectrum disorders.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Epigenetics

Background:

  • Fetal alcohol exposure impacts 1 in 100 children, a leading cause of mental retardation in the US.
  • Alcohol is known to affect cerebellum development and function, but molecular mechanisms remain unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms by which alcohol affects cerebellum development.
  • To examine the role of CREB binding protein (CBP) in the developing cerebellum following fetal alcohol exposure.

Main Methods:

  • Utilized rat models to study cerebellar development.
  • Assessed levels of CREB binding protein (CBP) and histone acetylation (H3 and H4) in the cerebellum after ethanol exposure.

Main Results:

  • CREB binding protein (CBP) is expressed in developing cerebellar neurons (granule and Purkinje cells).
  • Ethanol exposure during the third trimester-equivalent reduced CBP levels in the cerebellum.
  • Histone acetylation of H3 and H4 was decreased in the cerebellum of ethanol-exposed rats.

Conclusions:

  • Ethanol exposure decreases both the expression and function of CBP in the developing cerebellum.
  • Reduced CBP may underlie the motor coordination deficits observed in fetal alcohol spectrum disorders.
Abstract

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