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Expression profiling identifies strain-specific changes associated with ethanol withdrawal in mice.

G M Daniels1, K J Buck

  • 1Department of Behavioral Neuroscience, Portland Alcohol Research Center Oregon Health Sciences University, Portland Department of Veterans Affairs Medical Center, Portland, Oregon 97201, USA. danielsg@ohsu.edu

Genes, Brain, and Behavior
|July 31, 2003
PubMed
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Ethanol withdrawal severity differs between mouse strains due to distinct gene expression changes in the brain. DBA/2J mice show more widespread gene regulation during chronic ethanol withdrawal compared to C57BL/6J mice.

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Mice models are crucial for understanding human alcoholism and ethanol dependence.
  • Inbred mouse strains like DBA/2J and C57BL/6J exhibit varying behavioral responses to ethanol withdrawal.
  • Gene expression alterations are key to neuroadaptation during ethanol dependence and tolerance.

Purpose of the Study:

  • To investigate differential gene expression in the hippocampus of DBA/2J and C57BL/6J mice during ethanol withdrawal.
  • To identify specific molecular pathways involved in strain-dependent responses to ethanol withdrawal.

Main Methods:

  • Utilized cDNA microarrays to analyze gene expression profiles.
  • Compared gene expression in DBA/2J and C57BL/6J mice after chronic and acute ethanol exposure during withdrawal.

Related Experiment Videos

  • Focused analysis on the hippocampus.

    • Main Results:

    • Approximately 2% of surveyed genes showed significant differential expression in DBA/2J mice during chronic ethanol withdrawal.
    • Fewer than 1% of genes were altered in C57BL/6J mice under similar conditions or in DBA/2J mice during acute withdrawal.
    • Identified strain- and treatment-specific alterations in genes related to Janus kinase/signal transducers and activators of transcription (JAK/STAT) and mitogen-activated protein kinase (MAPK) pathways.
    • Observed differential expression of retinoic acid-mediated signaling genes exclusively in C57BL/6J mice.

    Conclusions:

    • Significant differences exist in cellular adaptation to ethanol between DBA/2J and C57BL/6J mouse strains.
    • The JAK/STAT and MAPK pathways are differentially regulated in DBA/2J mice during ethanol withdrawal.
    • The MAPK pathway and retinoic acid signaling are implicated in the C57BL/6J mouse response to ethanol withdrawal.