Journal
TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 28, Issue 4, Pages 166-172Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2007.02.006
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Funding
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH073853, P30MH040159, P50MH040159, R37MH073853] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS019576] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA013511] Funding Source: NIH RePORTER
- NIDA NIH HHS [DA-13511] Funding Source: Medline
- NIMH NIH HHS [MH-40159, MH-73853] Funding Source: Medline
- NINDS NIH HHS [NS-19576] Funding Source: Medline
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Drugs that act on dopamine neurotransmission are important tools for the management of multiple neuropsychiatric disorders. Classically, dopamine receptors have been shown to regulate cAMP-PKA (protein kinase A) and Ca2+ pathways through G-protein-mediated signaling. However, it has become apparent that, in addition to this canonical action, D-2-class dopamine receptors can function through a protein kinase B (Akt)-GSK-3 (glycogen synthase kinase 3) signaling cascade. This novel signaling mode involves the multifunctional scaffolding protein beta-arrestin 2, which has a role in G-protein-coupled receptor (GPCR) desensitization. In this article, we provide an overview of how this dual function of components of the GPCR desensitization machinery relates to dopamine-receptor-mediated responses and we summarize recent insights into the relevance of the Akt-GSK-3 signaling cascade for the expression of dopamine-associated behaviors and the actions of dopaminergic drugs.
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