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A beta-arrestin 2 signaling complex mediates lithium action on behavior.

Besides their role in desensitization, beta-arrestin 1 and 2 promote the formation of signaling complexes allowing G protein-coupled receptors (GPCR) to signal independently from G proteins. Here we show that lithium, a pharmacological agent used for the management of psychiatric disorders such as bipolar disorder, schizophrenia, and depression, regulates Akt/glycogen synthase kinase 3 (GSK3) signaling and related behaviors in mice by disrupting a signaling complex composed of Akt, beta-arrestin 2, and protein phosphatase 2A. When administered to beta-arrestin 2 knockout mice, lithium fails to affect Akt/GSK3 signaling and induce behavioral changes associated with GSK3 inhibition as it does in normal animals. These results point toward a pharmacological approach to modulating GPCR function that affects the formation of beta-arrestin-mediated signaling complexes.

Pubmed ID: 18191226


  • Beaulieu JM
  • Marion S
  • Rodriguiz RM
  • Medvedev IO
  • Sotnikova TD
  • Ghisi V
  • Wetsel WC
  • Lefkowitz RJ
  • Gainetdinov RR
  • Caron MG



Publication Data

January 11, 2008

Associated Grants

  • Agency: NIMH NIH HHS, Id: MH-40159
  • Agency: NIMH NIH HHS, Id: MH-73853
  • Agency: NINDS NIH HHS, Id: NS-19576

Mesh Terms

  • Animals
  • Antimanic Agents
  • Arrestins
  • Behavior, Animal
  • Brain
  • Cell Line
  • Down-Regulation
  • Glycogen Synthase Kinase 3
  • Humans
  • Lithium Chloride
  • Mice
  • Mice, Knockout
  • Mood Disorders
  • Motor Activity
  • Protein Phosphatase 2
  • Proto-Oncogene Proteins c-akt
  • Receptors, G-Protein-Coupled
  • Signal Transduction