Key Laboratory of Functional Proteomics of Guangdong Province, Key Laboratory of Mental Health of the Ministry of Education, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China; Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Nash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Neuropharmacology. 2020 Sep 15;175:108176. doi: 10.1016/j.neuropharm.2020.108176. Epub 2020 Jun 1.
Alcohol use disorder (AUD) places a tremendous burden on society, with approximately two billion alcohol users in the world. While most people drink alcohol recreationally, a subpopulation (3-5%) engages in reckless and compulsive drinking, leading to the development of AUD and alcohol dependence. The Ventral Tegmental Area (VTA)-Nucleus Accumbens (NAc) circuit has been shown to encode rewarding stimuli and drive individual alcohol drinking behavior. Our previous work successfully separated C57BL/6J isogenic mice into high or low alcohol drinking subgroups after a 12-day, two-bottle choice voluntary alcohol access paradigm. Electrophysiological studies revealed that low alcohol drinking mice exhibited elevated spontaneous and burst firing properties of their VTA dopamine (DA) neurons and specifically mimicking this pattern of activity in VTA-NAc neurons in high alcohol drinking mice using optogenetics decreased their alcohol preference. It is also known that VTA DA neurons encode the salience and rewarding properties of external stimuli while also regulating downstream dopamine concentrations. Here, as a follow-up to this study, we utilized Fast Scan Cyclic Voltammetry (FSCV) to examine dopamine release in the NAc shell and core between alcohol drinking groups. We observed dynamic changes of dopamine release in the core of high drinking mice, but failed to see widely significant differences of dopamine release in the shell of both groups, when compared with ethanol-naive controls. Overall, the present data suggest subregion-specific differences of evoked dopamine release in the NAc of low and high alcohol drinking mice, and may provide an anatomical substrate for individual alcohol drinking behavior. This article is part of the special issue on Stress, Addiction and Plasticity.
酒精使用障碍(AUD)给社会带来了巨大的负担,全世界约有 20 亿酒精使用者。虽然大多数人饮酒是为了娱乐,但有一部分人(3-5%)会鲁莽和强迫性地饮酒,导致 AUD 和酒精依赖的发展。腹侧被盖区(VTA)-伏隔核(NAc)回路已被证明可以编码奖励刺激,并驱动个体饮酒行为。我们之前的工作成功地将 C57BL/6J 同基因小鼠在 12 天的双瓶选择自愿酒精摄入范式后分为高或低酒精摄入亚组。电生理研究表明,低酒精摄入小鼠的 VTA 多巴胺(DA)神经元自发和爆发放电特性升高,并且使用光遗传学在高酒精摄入小鼠的 VTA-NAc 神经元中模拟这种活动模式会降低它们的酒精偏好。已知 VTA DA 神经元编码外部刺激的显着性和奖励属性,同时也调节下游多巴胺浓度。在这里,作为这项研究的后续,我们利用快速扫描循环伏安法(FSCV)检查了酒精摄入组之间 NAc 壳和核中的多巴胺释放。我们观察到高饮酒组小鼠核心中多巴胺释放的动态变化,但与乙醇未处理对照组相比,两组小鼠壳中多巴胺释放的广泛差异未观察到。总的来说,目前的数据表明,低和高酒精摄入小鼠的 NAc 中诱发的多巴胺释放存在亚区特异性差异,这可能为个体饮酒行为提供解剖学基础。本文是关于应激、成瘾和可塑性的特刊的一部分。