ArticleTranslational stroke research2018
Focal Ischaemic Infarcts Expand Faster in Cerebellar Cortex than Cerebral Cortex in a Mouse Photothrombotic Stroke Model.
Article in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke.Immunity, inflammation and disease · 2025Pooled it
- Inducing and monitoring photothrombotic stroke in anesthetic neuroprotection-free mice using functional photoacoustic microscopy.Neurophotonics · 2026Article
- Hemodynamic and Electrophysiological Progression of the Rose Bengal Photothrombotic Stroke Model in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- A step-by-step approach to minimally photothrombotic ischemic stroke in the hippocampal region that simulates human stroke.Lasers in medical science · 2025Article
- Effects and mechanisms of breastmilk stem cells in the treatment of white matter injury in newborn rats.Stem cell research & therapy · 2025Article
- TRPC Channels Activated by G Protein-Coupled Receptors Drive CaTranslational stroke research · 2024Article
- Microglia in Ischemic Stroke: Pathogenesis Insights and Therapeutic Challenges.Journal of inflammation research · 2024Review
- Gait disorders induced by photothrombotic cerebellar stroke in mice.Scientific reports · 2023Article
- Glial Cells Response in Stroke.Cellular and molecular neurobiology · 2023Review
- Differences in hippocampal plasticity and memory outcomes in anterior versus posterior cerebellar stroke.Neurobiology of disease · 2022Article
- Recovery of Post-Stroke Spatial Memory and Thalamocortical Connectivity Following Novel Glycomimetic and rhBDNF Treatment.International journal of molecular sciences · 2022Article
- Systemic immune responses after ischemic stroke: From the center to the periphery.Frontiers in immunology · 2022Review
- Activation of Galanin Receptor 1 with M617 Attenuates Neuronal Apoptosis via ERK/GSK-3β/TIP60 Pathway After Subarachnoid Hemorrhage in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Review
- Exploratory Investigation of Intestinal Structure and Function after Stroke in Mice.Mediators of inflammation · 2021Article
- Dual Functions of Microglia in Ischemic Stroke.Neuroscience bulletin · 2019Review
- Human Brain Region-Specific Alternative Splicing of TRPC3, the Type 3 Canonical Transient Receptor Potential Non-Selective Cation Channel.Cerebellum (London, England) · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally accepted that the cerebellum is particularly vulnerable to ischaemic injury, and this may contribute to the high mortality arising from posterior circulation strokes. However, this has not been systematically examined in an animal model. This study compared the development and resolution of matched photothrombotic microvascular infarcts in the cerebellar and cerebral cortices in adult 129/SvEv mice of both sexes. The photothrombotic lesions were made using tail vein injection of Rose Bengal with a 532 nm laser projected onto a 2 mm diameter aperture over the target region of the brain (with skull thinning). Infarct size was then imaged histologically following 2 h to 30-day survival using serial reconstruction of haematoxylin and eosin stained cryosections. This was complemented with immunohistochemistry for neuron and glial markers. At 2 h post-injury, the cerebellar infarct volume averaged ~ 2.7 times that of the cerebral cortex infarcts. Infarct volume reached maximum in the cerebellum in a quarter of the time (24 h) taken in the cerebral cortex (4 days). Remodelling resolved the infarcts within a month, leaving significantly larger residual injury volume in the cerebellum. The death of neurons in the core lesion at 2 h was confirmed by NeuN and Calbindin immunofluorescence, alongside activation of astrocytes and microglia. The latter persisted in the region within and surrounding the residual infarct at 30 days. This comparison of acute focal ischaemic injuries in cerebellar and cerebral cortices provides direct confirmation of exacerbation of neuropathology and faster kinetics in the cerebellum.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.