Genes and Gene Expression in the Brains of Human Alcoholics

  1. PETER R. DODD1,
  2. S. TRACEY BUCKLEY2,
  3. ALLISON L. ECKERT1,
  4. PHILOMENA F. FOLEY1,
  5. DAVID J. INNES1

Article first published online: 6 SEP 2006

DOI: 10.1196/annals.1369.010

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How to Cite

DODD, P. R., BUCKLEY, S. T., ECKERT, A. L., FOLEY, P. F. and INNES, D. J. (2006), Genes and Gene Expression in the Brains of Human Alcoholics. Annals of the New York Academy of Sciences, 1074: 104–115. doi: 10.1196/annals.1369.010

Author Information

  1. 1

    School of Molecular and Microbial Sciences, University of Queensland, Brisbane Q4072, Australia

  2. 2

    Perinatal Research Centre, Royal Brisbane and Women's Hospital, Brisbane 4072, Australia

*Address for correspondence: Peter R. Dodd, Ph.D., School of Molecular and Microbial Science, University of Queensland, Brisbane 4072, Australia. fax: +61-7-3365-4699.  e-mail: p.dodd@uq.edu.au

Publication History

  1. Issue published online: 6 SEP 2006
  2. Article first published online: 6 SEP 2006

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Keywords:

  • pathogenesis;
  • substance misuse and dependence;
  • brain damase;
  • phenotype;
  • cerebral cortex;
  • excitotoxicit

Abstract: Chronic alcohol misuse by human subjects leads to neuronal loss in regions such as the superior frontal cortex (SFC). Propensity to alcoholism is associated with several genes. γ-Aminobutyric acid (GABA)A receptor expression differs between alcoholics and controls, whereas glutamate receptor differences are muted. We determined whether genotype differentiated the regional presentation of GABAA and glutamate-NMDA (N-methyl-d-aspartate) receptors in SFC. Autopsy tissue was obtained from alcoholics without comorbid disease, alcoholics with liver cirrhosis, and matched controls. ADH1C, DRD2B, EAAT2, and APOE genotypes modulated GABAA-β subunit protein expression in SFC toward a less-effective form of the receptor. Most genotypes did not divide alcoholics and controls on glutamate-NMDA receptor pharmacology, although gender and cirrhosis did. Genotype may affect amino acid transmission locally to influence neuronal vulnerability.

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