Send to

Choose Destination
Addict Biol. 2010 Jul;15(3):299-303. doi: 10.1111/j.1369-1600.2010.00212.x. Epub 2010 Apr 29.

Ethanol-induced activation of AKT and DARPP-32 in the mouse striatum mediated by opioid receptors.

Author information

Laboratory of Clinical and Translational Studies, NIAAA, National Institutes of Health, Bethesda, MD 20892-1108, USA.


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center