Addictive drugs modulate GIRK-channel signaling by regulating RGS proteins.
Addictive drugs modulate GIRK-channel signaling by regulating RGS proteins.
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DOI：
10.1016/j.tips.2008.07.011
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发表时间：
2008-11
影响因子：
13.8
通讯作者：
Lüscher C
中科院分区：
文献类型：
--
作者：
Lomazzi M;Slesinger PA;Lüscher C
Regulator of G-protein signaling (RGS) proteins are strong modulators of G-protein-mediated pathways in the nervous system. One function of RGS proteins is to accelerate the activation–deactivation kinetics of G-protein-coupled inwardly rectifying potassium (GIRK) channels. The opening of GIRK channels reduces the firing rates of neurons. Recent studies suggest that RGS proteins also modulate the coupling efficiency between GABAB (gamma-amino butyric acid-type B) receptors and GIRK channels in dopamine neurons of the ventral tegmental area (VTA), the initial target for addictive drugs in the brain reward pathway. Chronic drug exposure can dynamically regulate the expression levels of RGS. Functional and behavioral studies now reveal that levels of RGS2 protein, through selective association with GIRK3, critically determine whether GABAB agonists are excitatory or inhibitory in the VTA. The regulation of RGS protein in the reward pathway may underlie adaptation to different types of addictive drugs.
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