Targeting the intracellular signaling "STOP" and "GO" pathways for the treatment of alcohol use disorders

被引:26
|
作者
Ron, Dorit [1 ]
Berger, Anthony [1 ]
机构
[1] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA
关键词
Alcohol; Addiction; Signaling; Translation; Medication Development; Fyn; mTOR; BDNF; GDNF; LONG-TERM POTENTIATION; NR2B-CONTAINING NMDA-RECEPTORS; CONDITIONED-PLACE PREFERENCE; ACTIVITY-DEPENDENT SECRETION; TYROSINE-PHOSPHATASE ALPHA; P75 NEUROTROPHIN RECEPTOR; DOPAMINE D-3 RECEPTOR; ANTI-ADDICTION DRUG; SYNAPTIC PLASTICITY; DORSOMEDIAL STRIATUM;
D O I
10.1007/s00213-018-4882-z
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In recent years, research has identified the molecular and neural substrates underlying the transition of moderate "social" consumption of alcohol to the characteristic alcohol use disorder (AUD) phenotypes including excessive and compulsive alcohol use which we define in the review as the GO signaling pathways. In addition, growing evidence points to the existence of molecular mechanisms that keep alcohol consumption in check and that confer resilience for the development of AUD which we define herein as the STOP signaling pathways. In this review, we focus on examples of the GO and the STOP intracellular signaling pathways and discuss our current knowledge of how manipulations of these pathways may be used for the treatment of AUD.
引用
收藏
页码:1727 / 1743
页数:17
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