Department of Diagnostic Radiology and Nuclear Medicine , University of Maryland School of Medicine, Baltimore, Maryland.
Core for Translational Research in Imaging at Maryland (C-TRIM) , University of Maryland School of Medicine, Baltimore, Maryland.
Alcohol Clin Exp Res. 2018 Apr;42(4):727-734. doi: 10.1111/acer.13611. Epub 2018 Mar 9.
Children with fetal alcohol spectrum disorders (FASD) often have deficits associated with multisensory processing. Because ethanol (EtOH) disrupts activity-dependent neuronal plasticity, a process that is essential for refining connections during cortical development, we hypothesize that early alcohol exposure results in alterations in multisensory cortical networks, which could explain the multisensory processing deficits seen in FASD. Here, we use a gyrencephalic animal model to test the prediction that early alcohol exposure alters the functional connectivity and microstructural features of the rostral posterior parietal cortex (PPr), a visual-tactile integrative area.
Ferrets were exposed to moderate doses of EtOH during the brain growth spurt period. Functional connectivity and microstructural features were assessed using resting-state functional magnetic resonance imaging and ex vivo diffusion kurtosis imaging (DKI), respectively, when the animals reached juvenile age and adulthood, respectively.
While the whole brain volume was smaller in alcohol-treated animals, the relative size of the frontal brain area was larger when compared to control animals. Altered functional connectivity was observed in alcohol-treated animals, where increased connectivity was observed between PPr and the region that provides its major visual inputs (the caudal portion of the parietal cortex), but not with the region that provides its major somatosensory inputs (tertiary somatosensory cortex). DKI revealed reduced microstructural tissue complexity in all investigated sensory areas of alcohol-treated animals.
In this study, we observed alterations in cortical functional connectivity and microstructural integrity in a cortical area involved in multisensory processing in a ferret FASD model. These findings indicate an alteration in cortical networks that may be related to the multisensory processing deficiencies observed in FASD.
患有胎儿酒精谱系障碍(FASD)的儿童通常存在与多感官处理相关的缺陷。由于乙醇(EtOH)会破坏活动依赖性神经元可塑性,而这一过程对于皮质发育过程中连接的精炼至关重要,因此我们假设早期酒精暴露会导致多感官皮质网络的改变,这可以解释 FASD 中观察到的多感官处理缺陷。在这里,我们使用一种脑回动物模型来检验以下预测:早期酒精暴露会改变额后顶叶皮质(PPr)的功能连接和微观结构特征,PPr 是一个视觉-触觉整合区域。
在大脑生长突增期间,给雪貂暴露于中等剂量的 EtOH。当动物达到幼年和成年时,分别使用静息状态功能磁共振成像和离体扩散峰度成像(DKI)评估功能连接和微观结构特征。
尽管酒精处理动物的全脑体积较小,但与对照动物相比,其额前脑区的相对大小更大。在酒精处理动物中观察到功能连接改变,其中 PPr 与提供其主要视觉输入的区域(顶叶皮质的尾部部分)之间的连接增加,但与提供其主要躯体感觉输入的区域(三级躯体感觉皮质)之间的连接没有改变。DKI 显示酒精处理动物的所有研究感觉区域的微观结构组织复杂性降低。
在这项研究中,我们在雪貂 FASD 模型中观察到参与多感官处理的皮质区域的皮质功能连接和微观结构完整性发生改变。这些发现表明皮质网络的改变可能与 FASD 中观察到的多感官处理缺陷有关。