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

Artikel i vetenskaplig tidskrift
Författare Susanne Jonsson
Nora Kerekes
Mia Ericson
Bo Söderpalm
Publicerad i Brain Research
Volym 1305
Nummer/häfte Supplement 1
Sidor pp. S27-S36
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor pp. S27-S36
Språk en
Länkar dx.doi.org/10.1016/j.brainres.2009....
Ämnesord glycinreceptor, genuttryck, etanol, råtta
Ämneskategorier Biologisk beroendeforskning, Beroendelära

Sammanfattning

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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