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

Cell | Jan 11, 2008

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 RIS Download

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 | beta-Arrestin 1 | beta-Arrestin 2 | beta-Arrestins

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Associated grants

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

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