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小鼠 Morris 水迷宫空间学习与记忆测定

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Assess spatial learning and memory in adult mice using hidden-platform training and platform-free probe trials, with escape latency, path length, swim velocity and target-quadrant time as readouts.

Scope and method

Sample：活体成年小鼠

学习与记忆评估

Reagents and materials

Procedure

  1. 训练试次

    每天从 N、S、E、W 四个象限边缘的 4 个不同起始位置释放每只小鼠。每次给予至多 100 s 寻找隐蔽平台；到达平台后停留 15 s。若小鼠在 100 s 内未找到平台，引导其到平台并停留 15 s。试次间将小鼠放回铺有干燥垫料的暂养笼，间隔 15–30 min。动物之间及不同训练日的起始位置应随机排列，避免形成固定位置策略。

  2. 无平台探测试次

    每个工作周结束时移除隐蔽平台，从原平台相对象限释放小鼠，自由游泳 100 s。使用 EthoVision 记录搜索路径。对目标象限的偏好反映空间记忆巩固。

  3. 数据分析

    使用 EthoVision 自动计算路径长度（cm）、游泳速度（cm/s）及各区域或象限停留时间。分析训练日之间的逃避潜伏期和路径长度，形成学习曲线；探测试验比较目标象限与其他象限的停留时间，并采用适合研究设计的统计检验。WT 小鼠的逃避潜伏期应随训练逐渐下降，探测试验对目标象限的偏好应达到 >25% 停留时间。KO 小鼠若存在空间学习障碍，可表现为逃避潜伏期延长或缺少象限偏好。

Quality control and readouts

水池直径 150 cm，水温 26 °C；平台直径 15 cm，位于水面下 1 cm。以 0.5% ACUSOL OP301 将水体调成不透明白色。同步记录游泳速度，结合路径长度及目标象限停留时间解释成绩。

训练期逃避潜伏期、路径长度和游泳速度；探测期目标象限停留时间及搜索路径。

Study design
重复训练后移除平台进行探测，比较训练过程中的学习曲线及探测试验的目标象限偏好。
Randomisation
每日从 N、S、E、W 四个方位下水，起始方位在动物和训练日之间随机排列。
Blinding
实验操作与数据分析对分组设盲。

References

  1. Sarah van Veen; Zsuzsanna Callaerts-Végh. Morris Water Maze: Spatial Learning and Memory Assessment in Mice. protocols.io, version 1, 2026-04-28. DOI:10.17504/protocols.io.5jyl84zk7g2w/v1.
  2. Pascual-Lucas Maria, Viana da Silva Silvia, Di Scala Marianna et al. Insulin-like growth factor 2 reverses memory and synaptic deficits in APP transgenic mice. 2014. DOI:10.15252/emmm.201404228; PMID:25100745.
  3. Salas Isabel H., Callaerts-Vegh Zsuzsanna, D’Hooge Rudi et al. Increased Insoluble Amyloid-β Induces Negligible Cognitive Deficits in Old App NL / NL Knock-In Mice. 2018. DOI:10.3233/JAD-180410; PMID:30320577.
  4. Wang Lu, Guo Lan, Lu Lin et al. Synaptosomal Mitochondrial Dysfunction in 5xFAD Mouse Model of Alzheimer's Disease. 2016. DOI:10.1371/journal.pone.0150441; PMID:26942905.
  5. Corbett Brian F., You Jason C., Zhang Xiaohong et al. ΔFosB regulates gene expression and cognitive dysfunction in a mouse model of Alzheimer’s disease. 2017. DOI:10.1016/j.celrep.2017.06.040; PMID:28700937.
  6. Hinrich Anthony J, Jodelka Francine M, Chang Jennifer L et al. Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides. 2016. DOI:10.15252/emmm.201505846; PMID:26902204.
  7. Wang Zhi-Hao, Gong Ke, Liu Xia et al. C/EBPβ regulates delta-secretase expression and mediates pathogenesis in mouse models of Alzheimer’s disease. 2018. DOI:10.1038/s41467-018-04120-z; PMID:29725016.
  8. Bailey et al. Effects of the C57BL/6 strain background on tauopathy progression in the rTg4510 mouse model. Molecular Neurodegeneration 2014;9:8. DOI:10.1186/1750-1326-9-8; PMID:24428919. Model/MWM applicability; the adopted procedure remains the separate protocols.io source version.
  9. Bouter et al. N-truncated amyloid beta (Abeta) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathologica 2013;126:189–205. DOI:10.1007/s00401-013-1129-2; PMID:23685882. Model/MWM applicability; source-specific assay parameters are not claimed to reproduce this article.
  10. PMID:40906458. Methods and Materials; Figure7 and APOE4 Aggregated Cognitive Deficits Induced by Blood-Derived Aβ. Humanized APOE4 recipients after marrow transplantation; the phenotype is not attributed to APOE4 genotype alone.

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