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Ethanol-induced activation of AKT and DARPP-32 in the mouse striatum mediated by opioid receptors
National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
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2010 (engelsk)Inngår i: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 15, nr 3, s. 299-303Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The reinforcing properties of ethanol are in part attributed to interactions between opioid and dopaminergic signaling pathways, but intracellular mediators of such interactions are poorly understood. Here we report that an acute ethanol challenge induces a robust phosphorylation of two key signal transduction kinases, AKT and DARPP-32, in the striatum of mice. Ethanol-induced AKT phosphorylation was blocked by the opioid receptor antagonist naltrexone but unaffected by blockade of dopamine D2 receptors via sulpiride. In contrast, DARPP-32 phosphorylation was abolished by both antagonists. These data suggest that ethanol acts via two distinct but potentially synergistic striatal signaling cascades. One of these is D2-dependent, while the other is not. These findings illustrate that pharmacology of ethanol reward is likely more complex than that for other addictive drugs.

sted, utgiver, år, opplag, sider
Wiley-Blackwell, 2010. Vol. 15, nr 3, s. 299-303
Emneord [en]
Dopamine, ethanol, opioids, signal transduction, striatum
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-101842DOI: 10.1111/j.1369-1600.2010.00212.xPubMedID: 20456289OAI: oai:DiVA.org:liu-101842DiVA, id: diva2:666728
Tilgjengelig fra: 2013-11-24 Laget: 2013-11-24 Sist oppdatert: 2018-01-11bibliografisk kontrollert

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