Selective changes of GABAA channel subunit mRNAs in the hippocampus and orbitofrontal cortex but not in prefrontal cortex of human alcoholics
- 1 The Division of Molecular Physiology and Neuroscience, Department of Neuroscience, Uppsala University, Uppsala, Sweden
- 2 The Division of Biological Research on Drug Dependence, Department of Pharmaceutical Bioscience, Uppsala University, Uppsala, Sweden
- 3 Institute of Biomedicine, Pharmacology, University of Helsinki, Finland
Alcohol dependence is a common chronic relapsing disorder. The development of alcohol dependence has been associated with changes in brain GABAA channel-mediated neurotransmission and plasticity. We have examined mRNA expression of the GABAA channel subunit genes in three brain regions in individuals with or without alcohol dependence using quantitative real-time PCR assay. The levels of selective GABAA channel subunit mRNAs were altered in specific brain regions in alcoholic subjects. Significant increase in the α1, α4, α5, β1, and γ1 subunit mRNAs in the hippocampal dentate gyrus region, and decrease in the β2 and δ subunit mRNAs in the orbitofrontal cortex were identified whereas no changes in the dorsolateral prefrontal cortex were detected. The data increase our understanding of the role of GABAA channels in the development of alcohol dependence.
Keywords: alcohol dependence, brain, GABAA channel, post-mortem
Citation: Jin Z, Bazov I, Kononenko O, Korpi ER, Bakalkin G and Birnir B (2012) Selective changes of GABAA channel subunit mRNAs in the hippocampus and orbitofrontal cortex but not in prefrontal cortex of human alcoholics. Front. Cell. Neurosci. 5:30. doi: 10.3389/fncel.2011.00030
Received: 12 October 2011;
Accepted: 14 December 2011;
Published online: 03 January 2012.
Reviewed by:
Istvan Mody, University of California Los Angeles, USA
Richard Olsen, University of California Los Angeles, USA
Copyright: © 2012 Jin, Bazov, Kononenko, Korpi, Bakalkin and Birnir. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
*Correspondence: Zhe Jin and Bryndis Birnir, The Division of Molecular Physiology and Neuroscience, Department of Neuroscience, BMC, Box 593, Uppsala University, Uppsala, Sweden. e-mail: zhe.jin@neuro.uu.se; bryndis.birnir@neuro.uu.se