Bordia Tanuja, Zahr Natalie M
Neuroscience Program, SRI International, Menlo Park, CA, United States.
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, United States.
Front Syst Neurosci. 2020 Dec 11;14:606345. doi: 10.3389/fnsys.2020.606345. eCollection 2020.
Post-mortem neuropathological and neuroimaging methods have demonstrated the vulnerability of the inferior colliculus to the sequelae of thiamine deficiency as occurs in Wernicke-Korsakoff Syndrome (WKS). A rich literature in animal models ranging from mice to monkeys-including our neuroimaging studies in rats-has shown involvement of the inferior colliculi in the neural response to thiamine depletion, frequently accomplished with pyrithiamine, an inhibitor of thiamine metabolism. In uncomplicated alcoholism (i.e., absent diagnosable neurological concomitants), the literature citing involvement of the inferior colliculus is scarce, has nearly all been accomplished in preclinical models, and is predominately discussed in the context of ethanol withdrawal. Our recent work using novel, voxel-based analysis of structural Magnetic Resonance Imaging (MRI) has demonstrated significant, persistent shrinkage of the inferior colliculus using acute and chronic ethanol exposure paradigms in two strains of rats. We speculate that these consistent findings should be considered from the perspective of the inferior colliculi having a relatively high CNS metabolic rate. As such, they are especially vulnerable to hypoxic injury and may be provide a common anatomical link among a variety of disparate insults. An argument will be made that the inferior colliculi have functions, possibly related to auditory gating, necessary for awareness of the external environment. Multimodal imaging including diffusion methods to provide more accurate visualization and quantification of the inferior colliculi may clarify the roles of brain stem nuclei such as the inferior colliculi in alcoholism and other neuropathologies marked by altered metabolism.
尸检神经病理学和神经影像学方法已证明，正如韦尼克-科尔萨科夫综合征（WKS）中所发生的那样，下丘对硫胺素缺乏的后遗症很敏感。从老鼠到猴子的动物模型中的大量文献——包括我们对大鼠的神经影像学研究——表明，下丘参与了对硫胺素耗竭的神经反应，硫胺素耗竭通常通过硫胺素代谢抑制剂吡硫胺来实现。在单纯性酒精中毒（即没有可诊断的神经系统伴随症状）中，引用下丘受累情况的文献很少，几乎所有研究都是在临床前模型中完成的，并且主要是在乙醇戒断的背景下进行讨论。我们最近使用基于体素的新型结构磁共振成像（MRI）分析的研究表明，在两种大鼠品系中，使用急性和慢性乙醇暴露范式时，下丘会出现显著且持续的萎缩。我们推测，这些一致的发现应从下丘具有相对较高的中枢神经系统代谢率这一角度来考虑。因此，它们特别容易受到缺氧损伤，并且可能在各种不同的损伤之间提供一个共同的解剖学联系。有人认为，下丘具有一些功能，可能与听觉门控有关，对于感知外部环境是必要的。包括扩散方法在内的多模态成像，以提供更准确的下丘可视化和量化，可能会阐明诸如下丘等脑干核在酒精中毒和其他以代谢改变为特征的神经病理学中的作用。
