Journal Article

Acute ethanol challenge inhibits glycogen synthase kinase-3β in the rat prefrontal cortex

Olga Neznanova, Karl Björk, Roberto Rimondini, Anita C. Hansson, Petri Hyytiä, Markus Heilig and Wolfgang H. Sommer

in International Journal of Neuropsychopharmacology

Published on behalf of International College of Neuropsychopharmacology

Volume 12, issue 2, pages 275-280
Published in print March 2009 | ISSN: 1461-1457
Published online March 2009 | e-ISSN: 1469-5111 | DOI: https://dx.doi.org/10.1017/S1461145708009620
Acute ethanol challenge inhibits glycogen synthase kinase-3β in the rat prefrontal cortex

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Abstract

Intracellular signalling pathways emerge as key mediators of the molecular and behavioural effects of addictive drugs including ethanol. Previously, we demonstrated that the innate high ethanol preference in AA rats is driven by dysfunctional endocannabinoid signalling in the medial prefrontal cortex (mPFC). Here, we report that acute ethanol challenge, at a dose commonly regarded as reinforcing, strongly phosphorylates glycogen synthase kinase-3β (GSK-3β) in this region with corresponding increased phosphorylation of AKT, a major regulator of GSK-3β. In the non-preferring counterpart ANA line we found a weaker, AKT-independent phosphorylation of GSK-3β by ethanol. Furthermore, AA rats showed rapid and transient dephosphorylation of ERK1/2 upon acute ethanol challenge in the medial prefrontal cortex (mPFC) and to a lesser degree in the nucleus accumbens; ANA rats were completely non-responsive for this mechanism. Together, these results identify candidate pathways for mediating high ethanol preference and emphasize the importance of the mPFC in controlling this behaviour.

Keywords: Alcohol use disorder; animal model; reinforcement; Western blotting

Journal Article.  2843 words.  Illustrated.

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