钒对非洲巨鼠海马trisins -aptic环神经元细胞结构的影响

O. Mustapha, Micheal Awala-Ajakaiye, Boluwatife Agbalu, S. Bello, M. Olude, James Olopade
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引用次数: 1

摘要

含钒的环境污染可能对非洲巨鼠(AGR)已知的独特神经属性(认知和嗅觉)造成神经毒性威胁。这种啮齿动物和人类生活在同一个生态区内。因此,对钒对这种啮齿动物影响的实验调查可能反映了人类中潜在的流行病学情景。这项工作旨在评估钒对海马神经元基础设施和电路的神经毒性作用,并提供其在AGR中重要病理的细胞相关性。12名成年男性agr被分为两组(n = 6/组;钒和控制)。每天给它们注射3 mg/kg的体内元氰酸钠和无菌水,持续14天,采集的脑进行组织学处理。利用尼氏和高尔基染色技术和体视学分析,我们证明了钒对海马三突触环AGR神经元结构的影响可能是钒诱导记忆缺陷的细胞机制。具体来说,最显著的病变出现在齿状回和CA3,神经元密度显著降低,细胞结构破坏,树突和轴突延伸丧失。同时,海马亚区CA2和CA4对钒诱导的神经毒性表现出区域特异性抗性。此外,对钒诱导的神经毒性的选择性易感性被引用。这项工作已经证明了钒对海马体亚区和AGR回路的神经毒性作用,并强调了其对其翻译目的的可能影响。这种啮齿动物可能是神经毒理学研究中评估记忆病理的合适模型
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Vanadium Impairs Neuronal Cytoarchitecture of the Hippocampal Trisyn-aptic Loop in the African Giant Rat (Cricetomys gambianus, Waterhouse)
Environmental pollution with vanadium may pose neurotoxicity threats to known unique neural attributes (cognition and olfaction) of the African giant rat (AGR). This rodent lives within the same ecological zones as the human populace. Thus, experimental investigations on the effect of vanadium on this rodent may mirror latent epidemiological scenarios in the human populace. This work was designed to evaluate the neurotoxic effect of vanadium on the hippocampal neuronal infrastructure and circuitry and provide cellular correlates to its significant pathologies in the AGR. Twelve adult male AGRs were assigned into two groups (n = 6/group; vanadium and control). They were dosed daily with 3 mg/kg body sodium metavanadate and sterile water for 14 days, respectively, and harvested brains were processed for histology. Using Nissl and Golgi staining techniques with stereological analysis, we demonstrated the effect of vanadium on AGR neuronal architecture of the hippocampal trisynaptic loop as a probable cellular mechanism of vanadium-induced memory deficits. Specifically, the most significant pathologies were seen in the dentate gyrus and CA3, with significantly decreased neuronal density disrupted cytoarchitecture and loss of dendritic arborisations and axonal extensions. At the same time, hippocampal subfields CA2 and CA4 showed region-specific resistance to vanadium-induced neurotoxicity. Furthermore, the selective vulnerability to vanadium-induced neurotoxicity is adduced. This work has demonstrated the neurotoxic effect of vanadium on the hippocampal subfields and circuitry in the AGR and highlighted its probable impact on their translational purposes. This rodent may be a suitable model for evaluating memory pathologies in neurotoxicological studies
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