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首页> 外文期刊>The European Journal of Neuroscience >Serotonin fibre sprouting and increase in serotonin transporter immunoreactivity in the CA1 area of hippocampus in a triple transgenic mouse model of Alzheimer's disease.
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Serotonin fibre sprouting and increase in serotonin transporter immunoreactivity in the CA1 area of hippocampus in a triple transgenic mouse model of Alzheimer's disease.

机译：在阿尔茨海默氏病的三重转基因小鼠模型中，海马CA1区的血清素纤维萌发和血清素转运蛋白免疫反应性增加。

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Alzheimer's disease (AD) is a neurodegenerative disease that deteriorates cognitive functions and associated brain regions such as the hippocampus, being the primary cause of dementia. Serotonin (5-HT) is widely present in the hippocampus, being an important neurotransmitter involved in learning and memory. Although recent evidence suggests alterations in 5-HT neurotransmission in AD, it is not clear how hippocampal 5-HT innervation is modified. Here, we studied hippocampal 5-HT innervation by analysing: (i) the expression, density and distribution of 5-HT transporter (SERT)-immunoreactive fibres; (ii) the specific morphological characteristics of serotonergic fibres and their relation to amyloid plaques; and (iii) the total number of 5-HT neurons within the raphe nuclei in triple transgenic mouse model of AD. We used quantitative light microscopy immunohistochemistry comparing transgenic and non-transgenic animals of different ages (3, 6, 9, 12 and 18 months). The transgenic animals showed a significant increase in SERT fibres in the hippocampus in a subfield-, strata- and age-specific manner. The increase in SERT fibres was specific to the CA1 stratum lacunosum-moleculare. An increase in SERT fibres in transgenic animals was observed at 3 months (by 61%) and at 18 months (by 74%). No changes, however, were found in the total number of raphe 5-HT neurons at any age. Our results indicate that triple transgenic mice display changes in the expression of SERT and increased SERT fibres sprouting, which may account for imbalanced serotonergic neurotransmission associated with (or linked to) AD cognitive impairment.
机译：阿尔茨海默氏病（AD）是一种神经退行性疾病，会恶化认知功能和相关的大脑区域（例如海马），这是痴呆症的主要原因。 5-羟色胺（5-HT）广泛存在于海马中，是参与学习和记忆的重要神经递质。尽管最近的证据表明AD中5-HT神经传递发生改变，但尚不清楚如何修饰海马5-HT神经支配。在这里，我们通过分析研究了海马5-HT的神经支配：（i）5-HT转运蛋白（SERT）-免疫反应性纤维的表达，密度和分布; （ii）血清素能纤维的具体形态特征及其与淀粉样斑块的关系; （iii）在AD的三重转基因小鼠模型中，缝核内的5-HT神经元总数。我们使用定量光学显微镜免疫组织化学比较了不同年龄（3、6、9、12和18个月）的转基因和非转基因动物。转基因动物以亚场，地层和年龄特定的方式显示海马中SERT纤维的显着增加。 SERT纤维的增加是特定于CA1腔层的分子。在3个月时（61％）和18个月时（74％）观察到转基因动物中SERT纤维的增加。但是，在任何年龄段的5-HT神经元总数都没有发现变化。我们的结果表明，三联转基因小鼠显示出SERT表达的变化和SERT纤维发芽的增加，这可能解释了与AD认知障碍相关（或相关）的血清素能神经传递失衡。

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