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The Inferior Colliculus in Alcoholism and Beyond
Frontiers in Systems Neuroscience ( IF 3.1 ) Pub Date : 2020-12-11 , DOI: 10.3389/fnsys.2020.606345
Tanuja Bordia 1 , Natalie M Zahr 1, 2
Affiliation  

Post-mortem neuropathological and in vivo 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 in vivo 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.

中文翻译:


酗酒及其他情况下的下丘



尸检神经病理学和体内神经影像学方法已证明下丘对硫胺素缺乏后遗症的脆弱性,如韦尼克-科萨科夫综合征 (WKS) 中发生的情况。从小鼠到猴子等动物模型的丰富文献(包括我们对大鼠的神经影像学研究)表明,下丘参与了硫胺素消耗的神经反应,这通常是通过硫胺素代谢抑制剂吡硫胺完成的。在无并发症的酒精中毒(即不存在可诊断的神经系统并发症)中,引用下丘受累的文献很少,几乎全部在临床前模型中完成,并且主要在乙醇戒断的背景下进行讨论。我们最近的工作使用新颖的、基于体素的结构磁共振成像(MRI)分析表明,在两种大鼠品系的急性和慢性乙醇暴露范例中,下丘出现显着、持续的收缩。我们推测这些一致的发现应该从具有相对较高的中枢神经系统代谢率的下丘的角度来考虑。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共同的解剖学联系。有人认为下丘具有感知外部环境所必需的功能,可能与听觉门控有关。多模态成像(包括扩散方法)可提供更准确的下丘体内可视化和量化,可以阐明脑干核(例如下丘)在酗酒和其他以代谢改变为标志的神经病理学中的作用。
更新日期:2020-12-11
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