Synaptic plasticity mechanisms common to learning and alcohol use disorder

被引:26
作者
Lovinger, David M. [1 ]
Abrahao, Karina P. [1 ]
机构
[1] NIAAA, Lab Integrat Neurosci, Div Intramural Clin & Biol Res, Bethesda, MD 20892 USA
关键词
LONG-TERM POTENTIATION; CHRONIC INTERMITTENT ETHANOL; METABOTROPIC GLUTAMATE RECEPTORS; NR2B-CONTAINING NMDA RECEPTORS; NUCLEUS-ACCUMBENS; HOMEOSTATIC PLASTICITY; GABAERGIC SYNAPSES; DENDRITIC SPINES; CENTRAL AMYGDALA; RAT HIPPOCAMPUS;
D O I
10.1101/lm.046722.117
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alcohol use disorders include drinking problems that span a range from binge drinking to alcohol abuse and dependence. Plastic changes in synaptic efficacy, such as long-term depression and long-term potentiation are widely recognized as mechanisms involved in learning and memory, responses to drugs of abuse, and addiction. In this review, we focus on the effects of chronic ethanol (EtOH) exposure on the induction of synaptic plasticity in different brain regions. We also review findings indicating that synaptic plasticity occurs in vivo during EtOH exposure, with a focus on ex vivo electrophysiological indices of plasticity. Evidence for effects of EtOH-induced or altered synaptic plasticity on learning and memory and EtOH-related behaviors is also reviewed. As this review indicates, there is much work needed to provide more information about the molecular, cellular, circuit, and behavioral consequences of EtOH interactions with synaptic plasticity mechanisms.
引用
收藏
页码:425 / 434
页数:10
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