模拟创伤性脑和神经损伤:来自斑马鱼的见解。

IF 3.5 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2025-03-27 eCollection Date: 2025-01-01 DOI:10.3389/fnmol.2025.1552885
Lada Murashova, Vyacheslav Dyachuk
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引用次数: 0

摘要

对哺乳动物来说,神经系统的创伤性损伤会造成严重后果,包括长期残疾、功能丧失和神经性疼痛。与哺乳动物相比,斑马鱼(Danio rerio)表现出明显增强的神经再生能力,这可归因于成年神经发生现象和损伤部位炎症反应的独特特征。大量研究证明了斑马鱼在不同实验损伤条件下的创伤后恢复,这大大提高了我们对这种动物神经再生的细胞和分子机制的理解。鉴于不同损伤部位、病变严重程度和有害物质在分子机制上的显著差异,选择合适的模型进行研究是至关重要的。本文讨论了一些模拟斑马鱼神经损伤的方法,并考虑了细胞相互作用在创伤后神经发生中的作用,重点关注动物的年龄和特定的损伤因素,这些因素可能用于选择某些神经系统病变的最佳模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modeling traumatic brain and neural injuries: insights from zebrafish.

A traumatic injury to the nervous system has significant consequences for mammals, including long-term disability, loss of functions, and neuropathic pain. In contrast to mammals, zebrafish (Danio rerio) exhibits a markedly enhanced neuroregenerative capacity, which can be attributed to the phenomenon of adult neurogenesis and to the distinctive characteristics of the inflammatory response at the injury site. The post-traumatic recovery of zebrafish under different experimental injury conditions was demonstrated in numerous studies, which has substantially advanced our understanding of the cellular and molecular mechanisms of neuroregeneration in this animal. In view of the significant differences in molecular mechanisms depending on the injury site, lesion severity, and harmful agents, selecting an appropriate model for investigations is of paramount importance. This review discusses some approaches to modeling neural injury in zebrafish and considers the effect of cellular interactions in post-traumatic neurogenesis, with focus on the animal's age and the specific damaging factor that may be used to select an optimum model for certain nervous system lesions.

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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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