期刊
TRENDS IN PHARMACOLOGICAL SCIENCES
卷 28, 期 4, 页码 166-172出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2007.02.006
关键词
-
资金
- 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
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据