Zhao Qingyu, Fritz Michael, Pfefferbaum Adolf, Sullivan Edith V, Pohl Kilian M, Zahr Natalie M
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, United States.
Neuroscience Program, SRI International, Menlo Park, CA, United States.
Front Neuroanat. 2018 Dec 11;12:108. doi: 10.3389/fnana.2018.00108. eCollection 2018.
Individuals aged 12-20 years drink 11% of all alcohol consumed in the United States with more than 90% consumed in the form of binge drinking. Early onset alcohol use is a strong predictor of future alcohol dependence. The study of the effects of excessive alcohol use on the human brain is hampered by limited information regarding the quantity and frequency of exposure to alcohol. Animal models can control for age at alcohol exposure onset and enable isolation of neural substrates of exposure to different patterns and quantities of ethanol (EtOH). As with humans, a frequently used binge exposure model is thought to produce dependence and affect predominantly corticolimbic brain regions. neuroimaging enables animals models to be examined longitudinally, allowing for each animal to serve as its own control. Accordingly, we conducted 3 magnetic resonance imaging (MRI) sessions (baseline, binge, recovery) to track structure throughout the brains of wild type Wistar rats to test the hypothesis that binge EtOH exposure affects specific brain regions in addition to corticolimbic circuitry. Voxel-based comparisons of 13 EtOH- vs. 12 water- exposed animals identified significant thalamic shrinkage and lateral ventricular enlargement as occurring with EtOH exposure, but recovering with a week of abstinence. By contrast, pretectal nuclei and superior and inferior colliculi shrank in response to binge EtOH treatment but did not recover with abstinence. These results identify brainstem structures that have been relatively underreported but are relevant for localizing neurocircuitry relevant to the dynamic course of alcoholism.
12至20岁的人群饮用了美国所有酒精饮料的11%,其中超过90%是以暴饮的形式摄入的。过早开始饮酒是未来酒精依赖的一个强有力的预测指标。由于关于酒精暴露的数量和频率的信息有限,过度饮酒对人类大脑影响的研究受到了阻碍。动物模型可以控制酒精暴露开始时的年龄,并能够分离出暴露于不同模式和数量乙醇(EtOH)的神经基质。与人类一样,常用的暴饮暴露模型被认为会产生依赖,并主要影响皮质边缘脑区。神经成像能够对动物模型进行纵向检查,使每只动物都能作为自身的对照。因此,我们进行了3次磁共振成像(MRI)检查(基线、暴饮、恢复),以追踪野生型Wistar大鼠全脑的结构,来检验暴饮EtOH暴露除了影响皮质边缘神经回路外还会影响特定脑区的假设。对13只暴露于EtOH的动物和12只暴露于水的动物进行基于体素的比较,发现丘脑显著萎缩和侧脑室扩大与EtOH暴露有关,但在禁欲一周后恢复。相比之下,顶盖前核以及上丘和下丘在暴饮EtOH处理后萎缩,但在禁欲后没有恢复。这些结果确定了脑干结构,这些结构相对较少被报道,但与定位与酒精中毒动态过程相关的神经回路有关。