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Glycine receptor expression in the forebrain of male AA/ANA rats

Journal article
Authors Susanne Jonsson
Nora Kerekes
Mia Ericson
Bo Söderpalm
Published in Brain Research
Volume 1305
Issue Supplement 1
Pages pp. S27-S36
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages pp. S27-S36
Language en
Keywords glycinreceptor, genuttryck, etanol, råtta
Subject categories Biological research on drug dependence, Substance Abuse


Ethanol is known to directly interact with the glycine receptor (GlyR). GlyRs are membrane proteins and are constituted as either α-homomers or α-β heteromers with a subunit stoichiometry of 2α3β. Previous studies by our group have suggested a role for GlyRs and its endogenous ligands glycine and taurine in the mesolimbic dopamine activating and reinforcing effects of ethanol. Here we use quantitative PCR (qPCR) to compare the relative GlyR expression in Alko Alcohol/Non-Alcohol (AA/ANA) rats. These animals have been selectively bred to create distinct populations regarding alcohol consumption and preference, presumably mainly due to genetic differences. The aim of this study was to examine the relative gene expression of GlyR subunits (α1–3 and β) in different brain areas and relate it to alcohol consumption. The hypothesis was that AA/ANA rats are differently disposed to ethanol consumption due to their GlyR set-ups and/or compositions. Results from the present study indicate that α2 is the most widely expressed α-subunit in the forebrain regions and that the α2β-heteromer seems to be the most common subunit composition in this part of the CNS. Despite displaying different drinking behaviours the anticipated differences in mRNA expression were few. However, correlations found between alcohol consumption and/or preference and GlyR expression support a role for GlyRs in alcohol consumption. Tentative differences between AA and ANA animals related to GlyR transmission could therefore lie in, for example, the regulation of the levels of the endogenous ligand(s) for the receptor or in mechanisms downstream to GlyR activation.

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