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bilateral common carotid artery stenosis C57BL/6 mouse

Bilateral common carotid artery stenosis in C57BL/6 mice produces chronic cerebral hypoperfusion with white-matter injury, glial activation and cognitive impairment. Lesion severity depends on posterior communicating artery patency and collateral vessels.

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。

Outcome measures

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。

Experimental animals

小鼠 Morris 水迷宫空间学习与记忆测定
Age
成年（来源未报告具体周龄）
Tissue
脑/海马（空间学习与记忆）
小鼠 Morris 水迷宫空间学习与记忆测定
Age
成年（来源未报告具体周龄）
Tissue
脑/海马（空间学习与记忆）

Experimental procedures

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。 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。 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。

Model identity

Model name
bilateral common carotid artery stenosis C57BL/6 mouse
Species
mouse
Taxonomy ID
10090
Strain
C57BL/6

Biological characteristics

Phenotype stage
Hypoperfusion is chronic; white-matter and cognitive changes develop over weeks.
Research questions
Chronic hypoperfusion; small-vessel disease; white-matter injury; collateral flow and vascular cognitive impairment.
Limitations
BCCAS is a hypoperfusion model rather than acute thromboembolic stroke. Posterior communicating artery patency and mouse strain determine lesion size, and surgery requires precise stenosis control.

Experimental methods

Experimental protocols

Reagents and materials

References

  1. Bonnin P, Kubis N, Charriaut-Marlangue C. Collateral Supply in Preclinical Cerebral Stroke Models.. Translational stroke research. 2022. PMID:34797519.
  2. Washida K, Hattori Y, Ihara M. Animal Models of Chronic Cerebral Hypoperfusion: From Mouse to Primate.. International journal of molecular sciences. 2019. PMID:31817864.
  3. NCBI Taxonomy official record: Mus musculus (house mouse), Taxonomy ID 10090.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. 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.
  14. ARRIVE 2.0 guidelines
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