Selective presynaptic degeneration in the synaptopathy associated with ME7-induced hippocampal pathology
Open accessAbstract
Intrahippocampal injection of the murine modified scrapie (ME7) induces a model of prion disease in vivo. Animals inoculated with ME7 brain homogenate were compared to controls at 8, 12 and 21 weeks. The data show that the accumulation of misfolded prion (PrP(Sc)) coincided with selective reduction in presynaptic protein expression early in disease. This loss is independent of a change in the number of cell bodies in CA3 that provide the major presynaptic input to the stratum radiatum. Electron microscopy of the stratum radiatum independently evidenced a progressive decrease in the number of synapses during disease. Further, the number of postsynaptic specializations lacking an intact presynaptic specialization increased from 12 to 21 weeks. This suggests that the presynaptic compartment is selectively disrupted when the previously reported first behavioural deficits are observed in this model. This synaptic pathology or "synaptopathy" may represent the earliest neuronal dysfunction in this and other protein misfolding induced neurodegenerative diseases.
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In a murine model of prion disease, electron microscopy revealed a selective loss of presynaptic compartments in CA3, while postsynaptic dendritic spines remained.
“For instance, in a murine model of prion disease, electron microscopy revealed a selective loss of presynaptic compartments in CA3, while postsynaptic dendritic spines remained (Gray et al., 2009).”
From Dendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice (2021) · cites this paper as Gray et al., 2009
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Self-citationDendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice
Walker, C. K., Greathouse, K. M., Boros, B. D., Poovey, E. H., Clearman, K. R., Ramdas, R., Muhammad, H. M., & Herskowitz, J. H. (2021) · Neuroscience · doi:10.1016/j.neuroscience.2020.12.006 · Cited by 27 · see citing works
Chouhan, J. K., Püntener, U., Booth, S. G., & Teeling, J. L. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.760721 · Cited by 24 · see citing works
- Authors
- Gray, B. C., Siskova, Z., Perry, V. H., & O'Connor, V.
- Affiliations
- University of Southampton (GB)
- Corresponding author
- O'Connor, Vincent
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 35
- Issue
- 1
- Pages
- 63-74
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1997907787
- Cited by
- 78
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 4 · 2017: 5 · 2016: 4 · 2015: 10 · 2014: 1 · 2013: 10 · 2012: 11
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- prion disease, synaptopathy, prion protein accumulation, hippocampus, CA3, stratum radiatum, synaptic loss, postsynaptic specialization, presynaptic proteins, neurodegeneration, protein misfolding
- MeSH terms
- Animals, Cell Count, Disease Models, Animal, Gene Expression Regulation, Hippocampus, Membrane Proteins, Mice, Inbred C57BL, Nerve Tissue Proteins, Phosphopyruvate Hydratase, Prions, Scrapie, Synapses, Time Factors, Prion Diseases, Presynaptic Terminals, Microscopy, Electron, Transmission, Mice
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