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

Karl Björk1, Anton Terasmaa, Hui Sun

  • 1Laboratory of Clinical and Translational Studies, NIAAA, National Institutes of Health, Bethesda, MD 20892-1108, USA.

Addiction Biology
|May 12, 2010
PubMed

Insights

Ethanol

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Ethanol's reinforcing effects involve opioid and dopaminergic pathways.
  • Intracellular mechanisms mediating these interactions are not well understood.

Purpose of the Study:

  • To investigate the intracellular signaling pathways affected by acute ethanol exposure.
  • To elucidate the roles of opioid and dopamine receptors in ethanol-induced signaling.

Main Methods:

  • Mice were administered acute ethanol.
  • Phosphorylation of AKT and DARPP-32 in the striatum was measured.
  • Effects of opioid receptor antagonist (naltrexone) and dopamine D2 receptor antagonist (sulpiride) were assessed.

Main Results:

  • Acute ethanol increased phosphorylation of AKT and DARPP-32 in the mouse striatum.
  • Ethanol-induced AKT phosphorylation was opioid-dependent but dopamine D2-independent.
  • DARPP-32 phosphorylation was dependent on both opioid and dopamine D2 receptors.

Conclusions:

  • Ethanol engages distinct, potentially synergistic striatal signaling cascades.
  • One cascade is dopamine D2-dependent, while the other is not.
  • The neuropharmacology of ethanol reward is complex and differs from other addictive drugs.

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