Demyelination of the hippocampus is prominent in the cuprizone model
Abstract
In multiple sclerosis demyelination not only affects the white matter, but also the grey matter of the brain. We have previously reported that in the murine cuprizone model for demyelination lesions occur in addition to the corpus callosum also in the neocortex and hippocampus. In the current study, we provide a detailed characterization of hippocampal demyelination in the cuprizone model. Male C57BL/6 mice were challenged with 0.2% cuprizone for 6 weeks. Defined structures within the hippocampus were investigated at week 0 (control), 3, 4, 4.5, 5, 5.5, and 6. Demyelination affected all hippocampal structures analyzed and was complete after 6 weeks of cuprizone treatment. Between the distinct hippocampal structures the temporal pattern of demyelination varied considerably. Furthermore, infiltration of activated microglia as well as astrogliosis was detected. In summary, cuprizone feeding provides a useful model for studying demyelination processes in the mouse hippocampus.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Cuprizone-dependent demyelination is massive within the corpus callosum but also occurs within additional brain regions such as the cortex and hippocampus.
“cuprizone-dependent demyelination is massive within the corpus callosum but also occurs within additional brain regions such as the cortex and hippocampus (Koutsoudaki et al. 2009; Skripuletz et al. 2008; Steelman et al. 2012).”
From Cuprizone-Dependent De/Remyelination Responses and Functional Correlates in Mouse Strains Adopted to Model Relapsing, Chronic and Progressive Experimental Autoimmune Encephalomyelitis (2021) · cites this paper as Koutsoudaki et al. 2009
Demyelination may also be detected in other brain regions such as hippocampus, basal ganglia, and cerebellum.
“Furthermore, demyelination may also be detected in other brain regions such as hippocampus, basal ganglia, and cerebellum (Koutsoudaki et al., 2009; Pott et al., 2009; Skripuletz et al., 2010a).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Koutsoudaki et al., 2009
Cites
Matsushima, G. K., & Morell, P. (2001) · Brain Pathology · doi:10.1111/j.1750-3639.2001.tb00385.x · Cited by 984 · see citing works
Burgess, A., Wainwright, S. R., Shihabuddin, L. S., Rutishauser, U., Seki, T., & Aubert, I. (2008) · Developmental Neurobiology · doi:10.1002/dneu.20681 · Cited by 65 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned
Gudi, V., Gingele, S., Skripuletz, T., & Stangel, M. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00073 · Cited by 375 · see citing works
“Demyelination peaks between 4.5 and 5 weeks of cuprizone exposure in the CC and between 5 and 6 weeks in the cortex and hippocampus (Hiremath et al., 1998; Matsushima and Morell, 2001; Skripuletz et al., 2008; Gudi et al., 2009; Koutsoudaki et al., 2009).”
BackgroundInfluentialSelf-citationThe benefits and detriments of macrophages/microglia in models of multiple sclerosis
Rawji, K. S., & Yong, V. W. (2013) · Clinical and Developmental Immunology · doi:10.1155/2013/948976 · Cited by 217 · see citing works
“Significant M/M accumulation has been reported in lesions in this model, allowing the specific involvement of these cells in demyelination and remyelination to be examined [59, 61, 65–68].”
BackgroundPolysialic acid in brain development and synaptic plasticity
Hildebrandt, H., & Dityatev, A. (2013) · Topics in current chemistry · doi:10.1007/128_2013_446 · Cited by 94 · see citing works
Self-citationMakinodan, M., Yamauchi, T., Tatsumi, K., Okuda, H., Takeda, T., Kiuchi, K., Sadamatsu, M., Wanaka, A., & Kishimoto, T. (2009) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2009.05.006 · Cited by 78 · see citing works
Tezuka, T., Tamura, M., Kondo, M. A., Sakaue, M., Okada, K., Takemoto, K., Fukunari, A., Miwa, K., Ohzeki, H., Kano, S.-I., et al. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.07.003 · Cited by 64 · see citing works
Buonvicino, D., Ranieri, G., & Chiarugi, A. (2021) · Neurotoxicity Research · doi:10.1007/s12640-021-00331-3 · Cited by 8 · see citing works
- Authors
- Koutsoudaki, P. N., Skripuletz, T., Gudi, V., Moharregh-Khiabani, D., Hildebrandt, H., Trebst, C., & Stangel, M.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Corresponding author
- Stangel, Martin
- ORCID
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 451
- Issue
- 1
- Pages
- 83-88
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W1989398840
- Cited by
- 119
- References
- 2
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 6 · 2023: 9 · 2022: 8 · 2021: 5 · 2020: 11 · 2019: 6 · 2018: 10 · 2017: 9 · 2016: 3 · 2015: 10 · 2014: 3 · 2013: 10 · 2012: 3
- FWCI
- 4.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Marie Curie (MST-CT-2005 021014)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- cuprizone model, multiple sclerosis, microglial activation, astrocyte activation, C57BL/6 mice
- MeSH terms
- Animals, Astrocytes, Chelating Agents, Cuprizone, Demyelinating Diseases, Disease Models, Animal, Gliosis, Hippocampus, Immunohistochemistry, Male, Mice, Inbred C57BL, Nerve Fibers, Myelinated, Nerve Tissue Proteins, Neurotoxins, Wallerian Degeneration, Biomarkers, Microglia, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
