Deletion of GSK3β in D2R-expressing neurons reveals distinct roles for β-arrestin signaling in antipsychotic and lithium action.

@article{Urs2012DeletionOG,
  title={Deletion of GSK3β in D2R-expressing neurons reveals distinct roles for β-arrestin signaling in antipsychotic and lithium action.},
  author={Nikhil M Urs and Joshua C. Snyder and Jacob Pade Rams\oe Jacobsen and Sean M. Peterson and Marc G. Caron},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2012},
  volume={109 50},
  pages={20732-7}
}
Several studies in rodent models have shown that glycogen synthase kinase 3 β (GSK3β) plays an important role in the actions of antispychotics and mood stabilizers. Recently it was demonstrated that GSK3β through a β-arrestin2/protein kinase B (PKB or Akt)/protein phosphatase 2A (PP2A) signaling complex regulates dopamine (DA)- and lithium-sensitive behaviors and is required to mediate endophenotypes of mania and depression in rodents. We have previously shown that atypical antipsychotics… CONTINUE READING

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