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匹罗卡品癫痫模型中海马硬化:成年 NMRI 品系小鼠含肽神经元的存活和学习记忆障碍。

Hippocampal Sclerosis in Pilocarpine Epilepsy: Survival of Peptide-Containing Neurons and Learning and Memory Disturbances in the Adult NMRI Strain Mouse.

机构信息

Department of Anatomy, Albert Szent-Györgyi Faculty of Medicine, University of Szeged, Kossuth L. sgt. 38, H-6724 Szeged, Hungary.

Department of Medical Chemistry, University of Szeged, Dóm tér. 8, H-6720 Szeged, Hungary.

出版信息

Int J Mol Sci. 2021 Dec 24;23(1):204. doi: 10.3390/ijms23010204.

Abstract

The present experiments reveal the alterations of the hippocampal neuronal populations in chronic epilepsy. The mice were injected with a single dose of pilocarpine. They had status epilepticus and spontaneously recurrent motor seizures. Three months after pilocarpine treatment, the animals were investigated with the Barnes maze to determine their learning and memory capabilities. Their hippocampi were analyzed 2 weeks later (at 3.5 months) with standard immunohistochemical methods and cell counting. Every animal displayed hippocampal sclerosis. The neuronal loss was evaluated with neuronal-N immunostaining, and the activation of the microglia was measured with Iba1 immunohistochemistry. The neuropeptide Y, parvalbumin, and calretinin immunoreactive structures were qualitatively and quantitatively analyzed in the hippocampal formation. The results were compared statistically to the results of the control mice. We detected neuronal loss and strongly activated microglia populations. Neuropeptide Y was significantly upregulated in the sprouting axons. The number of parvalbumin- and calretinin-containing interneurons decreased significantly in the Ammon's horn and dentate gyrus. The epileptic animals displayed significantly worse learning and memory functions. We concluded that degeneration of the principal neurons, a numerical decrease of PV-containing GABAergic neurons, and strong peptidergic axonal sprouting were responsible for the loss of the hippocampal learning and memory functions.

摘要

本实验揭示了慢性癫痫中海马神经元群体的改变。小鼠接受了匹鲁卡品的单次注射。它们发生了癫痫持续状态和自发性反复运动性发作。在匹鲁卡品治疗 3 个月后,用巴恩斯迷宫对动物进行了调查,以确定它们的学习和记忆能力。2 周后(在 3.5 个月时)用标准免疫组织化学方法和细胞计数分析其海马。每只动物都显示出海马硬化。用神经元-N 免疫染色评估神经元丢失,并用 Iba1 免疫组织化学测量小胶质细胞的激活。在海马结构中定性和定量分析神经肽 Y、副钙蛋白和钙结合蛋白免疫反应性结构。将结果与对照小鼠的结果进行统计学比较。我们检测到神经元丢失和强烈激活的小胶质细胞群体。神经肽 Y 在发芽轴突中明显上调。在齿状回和 ammon 的 horn 中,含有副钙蛋白和钙结合蛋白的中间神经元的数量明显减少。癫痫动物的学习和记忆功能明显下降。我们得出结论,主要神经元的退化、PV 含量 GABA 能神经元数量的减少以及强烈的肽能轴突发芽是导致海马学习和记忆功能丧失的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dc6/8745054/90a6e3ddabca/ijms-23-00204-g001.jpg

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