阿尔茨海默病动物模型学习过程中脑组织中Arc/Arg3.1的表达

Maria V. Ryazanova, Anton S. Averchuk, Alla V. Stavrovskaya, Natalia A. Rozanova, Svetlana V. Novikova, Alla B. Salmina
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 Objective: to evaluate the changes in Arc/Arg3.1 expression in the post-mitotic neurons and to assess the proliferative activity of the neurogenic niche cells in Alzheimer's disease animal models.
 Materials and methods. We divided the C57Bl/6В mice into 2 groups: experimental (n = 15) and control (n = 15). The experimental group were injected with the amyloid- oligomers 2535 in their CA1 hippocampal region while the control mice received normal saline injections in the same region. Passive Avoidance Test (PAT) was used to assess the cognitive functions from the day 9 after the intervention. One hour after each test session we collected the samples of brain tissues to immunohistochemically assess them for the Arc/Arg3.1 expression and PCNA cell proliferation marker.
 Results. At day 11 the count of Arc/Arg3.1+NeuN+ cells in the subgranular zone had significantly increased. In animal neurodegeneration models the 1st and 2nd PAT sessions were associated with a significant increase in Arc/Arg3.1+NeuN+ cells, although by the day 11 their count significantly decreased. The count of Arc/Arg3.1+ cells in the subventricular and subgranular zones had increased after the 3rd PAT session in the control group while in Alzheimer's disease animal models this was observed only after the 2nd PAT session. Preserved Arc/Arg3.1 expression in the subventricular zone is associated with the increased PCNA cell prolifera- tion marker expression. At the same time, the toxic effect of the amyloid- oligomers suppressed the cells' proliferative activity in the subgranular zone at day 9.
 Conclusions. Despite the toxic effect of the amyloid- oligomers 2535, the post-mitotic neurons of the neurogenic niches retained the ability to express Arc/Arg3.1 in vivo. The obtained results show a transient increase in sensitivity of the post-mitotic neurons of the neurogenic niches for the learning stimuli in the early stages of the Alzheimer-type neurodegeneration.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Arc/Arg3.1 expression in the brain tissues during the learning process in Alzheimer's disease animal models\",\"authors\":\"Maria V. Ryazanova, Anton S. Averchuk, Alla V. Stavrovskaya, Natalia A. Rozanova, Svetlana V. Novikova, Alla B. Salmina\",\"doi\":\"10.54101/acen.2023.3.6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction. Arc/Arg3.1 is a common marker of neuronal activation for learning and memorizing. Some experimental data show the Arc/Arg3.1 expression in the post-mitotic neurons of the neurogenic niches. At the same time, we still have to understand the importance of such an expression for neurogenesis induced by the learning or memorizing processes, in health and in disease.
 Objective: to evaluate the changes in Arc/Arg3.1 expression in the post-mitotic neurons and to assess the proliferative activity of the neurogenic niche cells in Alzheimer's disease animal models.
 Materials and methods. We divided the C57Bl/6В mice into 2 groups: experimental (n = 15) and control (n = 15). The experimental group were injected with the amyloid- oligomers 2535 in their CA1 hippocampal region while the control mice received normal saline injections in the same region. Passive Avoidance Test (PAT) was used to assess the cognitive functions from the day 9 after the intervention. One hour after each test session we collected the samples of brain tissues to immunohistochemically assess them for the Arc/Arg3.1 expression and PCNA cell proliferation marker.
 Results. At day 11 the count of Arc/Arg3.1+NeuN+ cells in the subgranular zone had significantly increased. In animal neurodegeneration models the 1st and 2nd PAT sessions were associated with a significant increase in Arc/Arg3.1+NeuN+ cells, although by the day 11 their count significantly decreased. The count of Arc/Arg3.1+ cells in the subventricular and subgranular zones had increased after the 3rd PAT session in the control group while in Alzheimer's disease animal models this was observed only after the 2nd PAT session. Preserved Arc/Arg3.1 expression in the subventricular zone is associated with the increased PCNA cell prolifera- tion marker expression. At the same time, the toxic effect of the amyloid- oligomers suppressed the cells' proliferative activity in the subgranular zone at day 9.
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引用次数: 0

摘要

介绍。Arc/Arg3.1是学习和记忆神经元激活的常见标记物。一些实验数据表明,Arc/Arg3.1在神经源性神经龛的有丝分裂后神经元中表达。同时,我们还必须了解这种表达对于由学习或记忆过程诱导的神经发生,在健康和疾病中的重要性。目的:探讨阿尔茨海默病动物模型中有丝分裂后神经元中Arc/Arg3.1表达的变化及神经源性生态位细胞的增殖活性。 材料和方法。我们将C57Bl/6В小鼠分为实验组(n = 15)和对照组(n = 15)。实验组小鼠在CA1海马区注射淀粉样蛋白低聚物2535,对照组小鼠在CA1海马区注射生理盐水。从干预后第9天开始,采用被动回避测验(PAT)评估认知功能。每次测试1小时后,我们收集脑组织样本,用免疫组织化学方法评估它们的Arc/Arg3.1表达和PCNA细胞增殖标志物。 结果。第11天,亚颗粒区Arc/Arg3.1+NeuN+细胞数量显著增加。在动物神经变性模型中,第1次和第2次PAT与Arc/Arg3.1+NeuN+细胞的显著增加有关,尽管到第11天它们的计数显著减少。在对照组中,第三次PAT后脑室下和颗粒下区Arc/Arg3.1+细胞计数增加,而在阿尔茨海默病动物模型中,这种情况仅在第二次PAT后观察到。在脑室下区保存的Arc/Arg3.1表达与PCNA细胞增殖标志物表达的增加有关。同时,淀粉样蛋白低聚物的毒性作用在第9天抑制了细胞在亚颗粒区的增殖活性。 结论。尽管淀粉样蛋白低聚物2535具有毒性作用,但神经源性神经龛的有丝分裂后神经元在体内保留了表达Arc/Arg3.1的能力。所获得的结果表明,在阿尔茨海默型神经变性的早期阶段,神经源性小生境的有丝分裂后神经元对学习刺激的敏感性有短暂的增加。
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Arc/Arg3.1 expression in the brain tissues during the learning process in Alzheimer's disease animal models
Introduction. Arc/Arg3.1 is a common marker of neuronal activation for learning and memorizing. Some experimental data show the Arc/Arg3.1 expression in the post-mitotic neurons of the neurogenic niches. At the same time, we still have to understand the importance of such an expression for neurogenesis induced by the learning or memorizing processes, in health and in disease. Objective: to evaluate the changes in Arc/Arg3.1 expression in the post-mitotic neurons and to assess the proliferative activity of the neurogenic niche cells in Alzheimer's disease animal models. Materials and methods. We divided the C57Bl/6В mice into 2 groups: experimental (n = 15) and control (n = 15). The experimental group were injected with the amyloid- oligomers 2535 in their CA1 hippocampal region while the control mice received normal saline injections in the same region. Passive Avoidance Test (PAT) was used to assess the cognitive functions from the day 9 after the intervention. One hour after each test session we collected the samples of brain tissues to immunohistochemically assess them for the Arc/Arg3.1 expression and PCNA cell proliferation marker. Results. At day 11 the count of Arc/Arg3.1+NeuN+ cells in the subgranular zone had significantly increased. In animal neurodegeneration models the 1st and 2nd PAT sessions were associated with a significant increase in Arc/Arg3.1+NeuN+ cells, although by the day 11 their count significantly decreased. The count of Arc/Arg3.1+ cells in the subventricular and subgranular zones had increased after the 3rd PAT session in the control group while in Alzheimer's disease animal models this was observed only after the 2nd PAT session. Preserved Arc/Arg3.1 expression in the subventricular zone is associated with the increased PCNA cell prolifera- tion marker expression. At the same time, the toxic effect of the amyloid- oligomers suppressed the cells' proliferative activity in the subgranular zone at day 9. Conclusions. Despite the toxic effect of the amyloid- oligomers 2535, the post-mitotic neurons of the neurogenic niches retained the ability to express Arc/Arg3.1 in vivo. The obtained results show a transient increase in sensitivity of the post-mitotic neurons of the neurogenic niches for the learning stimuli in the early stages of the Alzheimer-type neurodegeneration.
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Annals of Clinical and Experimental Neurology
Annals of Clinical and Experimental Neurology Medicine-Neurology (clinical)
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0.80
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32
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