A model of global cerebral ischemia in C57 BL/6 mice
Open accessAbstract
A reproducible model of global cerebral ischemia in mice is essential for elucidating the molecular mechanism of ischemic neuronal injury. Such a model is particularly important in the mouse because many genetically engineered mutant animals are available. In C57BL/6 and SV129/EMS mice, we evaluated a three-vessel occlusion model. Occlusion of the basilar artery with a miniature clip was followed by bilateral carotid occlusion. The mean cortical cerebral blood flow was reduced to less than 10% of the preischemic value, and the mean anoxic depolarization was attained within 1 minute. In C57BL/6 mice, there was CA1 hippocampal neuronal degeneration 4 days after ischemia. Neuronal damage depended upon ischemic duration: the surviving neuronal count was 78.5 ± 8.5% after 8-minute ischemia and 8.4 ± 12.7% after 14-minute ischemia. In SV129/EMS mice, similar neuronal degeneration was not observed after 14-minute ischemia. The global ischemia model in C57BL/6 mice showed high reproducibility and consistent neuronal injury in the CA1 sector, indicating that comparison of ischemic outcome between wild-type and mutant mice could provide meaningful data using the C57BL/6 genetic background. Strain differences in this study highlight the need for consideration of genetic background when evaluating ischemia experiments in mice.
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Studies have demonstrated delayed loss of C57BL/6 mouse cortical neurons caused by brief global ischemia using similar models.
“However, studies have also demonstrated delayed loss of C57BL/6 mouse cortical neurons caused by brief global ischemia using similar models (Olsson et al., 2003;Yonekura et al., 2004).”
From Two-Photon Imaging of Stroke Onset<i>In Vivo</i>Reveals That NMDA-Receptor Independent Ischemic Depolarization Is the Major Cause of Rapid Reversible Damage to Dendrites and Spines (2008) · cites this paper as Yonekura et al., 2004
The Discussion reports ischemic injury in the cortex of C57BL/6 mice after a brief global-ischemia procedure, but says cortical injury was inconsistent in frequency and intensity. The ‘Ischemic injury in other regions’ section reports TUNEL-positive cells in cortical layers after 14-minute ischemia; the clear temporal evidence for delayed neuronal loss, however, concerns hippocampal CA1 neurons, not cortical neurons. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMost previous work in rodent global ischemia concerns the selective delayed death of hippocampal CA1 neurons triggered by ischemia in excess of 10 min.
“Most previous work in rodent global ischemia concerns the selective delayed death of hippocampal CA1 neurons triggered ischemia in excess of 10 min (Traystman, 2003;Yonekura et al., 2004).”
From Two-Photon Imaging of Stroke Onset<i>In Vivo</i>Reveals That NMDA-Receptor Independent Ischemic Depolarization Is the Major Cause of Rapid Reversible Damage to Dendrites and Spines (2008) · cites this paper as Yonekura et al., 2004
The Abstract says numerous studies have examined selective ischemic injury in hippocampal CA1 neurons. The CA1 injury section reports delayed injury after ischemia lasting longer than 10 minutes in this study's C57BL/6 mice, but does not establish that this duration characterizes most previous rodent work; the Discussion says the duration required in these mice was longer than previously reported for rats and gerbils. Page numbers were not provided in our copy. (LLM, conf=0.88)
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Cites
The Mouse Brain in Stereotaxic Coordinates
Paxinos, G. (2001) · Cited by 12,859 · see citing works
mouse brain in stereotaxic coordinates
Franklin, K. B. J., & Paxinos, G. (1997) · Cited by 3,258 · see citing works
Delayed neuronal death in the gerbil hippocampus following ischemia
Kirino, T. (1982) · Brain Research · doi:10.1016/0006-8993(82)90833-2 · Cited by 2,856 · see citing works
Self-citationEffects of Cerebral Ischemia in Mice Deficient in Neuronal Nitric Oxide Synthase
Huang, Z., Huang, P. L., Panahian, N., Dalkara, T., Fishman, M. C., & Moskowitz, M. A. (1994) · Science · doi:10.1126/science.7522345 · Cited by 1,562 · see citing works
Nakatomi, H., Kuriu, T., Okabe, S., Yamamoto, S.-I., Hatano, O., Kawahara, N., Tamura, A., Kirino, T., & Nakafuku, M. (2002) · Cell · doi:10.1016/s0092-8674(02)00862-0 · Cited by 1,416 · see citing works
Self-citationSmith, M., Auer, R. N., & Siesj�, B. K. (1984) · Acta Neuropathologica · doi:10.1007/bf00690397 · Cited by 955 · see citing works
Gene-targeting studies of mammalian behavior: is it the mutation or the background genotype?
Gerlai, R. (1996) · Trends in Neurosciences · doi:10.1016/s0166-2236(96)20020-7 · Cited by 881 · see citing works
Moderate hyperglycemia augments ischemic brain damage
Pulsinelli, W. A., Waldman, S., Rawlinson, D. G., & Plum, F. (1982) · Neurology · doi:10.1212/wnl.32.11.1239 · Cited by 725 · see citing works
Schauwecker, P. E., & Steward, O. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.8.4103 · Cited by 510 · see citing works
Kitagawa, K., Matsumoto, M., Yang, G., Mabuchi, T., Yagita, Y., Hori, M., & Yanagihara, T. (1998) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/00004647-199805000-00012 · Cited by 250 · see citing works
Fujii, M., Hara, H., Meng, W., Vonsattel, J. P., Huang, Z., & Moskowitz, M. A. (1997) · Stroke · doi:10.1161/01.str.28.9.1805 · Cited by 242 · see citing works
Panahian, N., Yoshida, T., Huang, P. L., Hedley‐Whyte, E. T., Dalkara, T., Fishman, M. C., & Moskowitz, M. A. (1996) · Neuroscience · doi:10.1016/0306-4522(95)00563-3 · Cited by 162 · see citing works
Kawai, K., Nitecka, L., Ruetzler, C. A., et al. (1992) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.1992.34 · Cited by 158 · see citing works
Wellons, J. C., Sheng, H., Laskowitz, D. T., Mackensen, G. B., Pearlstein, R. D., & Warner, D. S. (2000) · Brain Research · doi:10.1016/s0006-8993(00)02216-2 · Cited by 115 · see citing works
Kawahara, N., Ruetzler, C. A., & KLATZO, I. (1995) · Neurological Research · doi:10.1080/01616412.1995.11740281 · Cited by 109 · see citing works
Self-citationCharacterization of a recovery global cerebral ischemia model in the mouse
Sheng, H., Laskowitz, D. T., Pearlstein, R. D., et al. (1999) · Journal of Neuroscience Methods · doi:10.1016/s0165-0270(99)00018-7 · Cited by 64 · see citing works
Kawahara, N., Kawai, K., Toyoda, T., et al. (2002) · Neuroscience Letters · doi:10.1016/s0304-3940(02)00101-5 · Cited by 19 · see citing works
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Murphy, T. H., Li, P., Betts, K., & Liu, R. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.5128-07.2008 · Cited by 261 · see citing works
“However, studies have also demonstrated delayed loss of C57BL/6 mouse cortical neurons caused by brief global ischemia using similar models (Olsson et al., 2003; Yonekura et al., 2004).”
Background
- Authors
- Yonekura, I., Kawahara, N., Nakatomi, H., Furuya, K., & Kirino, T.
- Affiliations
- Japan Science and Technology Agency (JP)
- Corresponding author
- Kawahara, Nobutaka
- ORCID
- Nakatomi, Hirofumi
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2004-02
- Volume
- 24
- Issue
- 2
- Pages
- 151-158
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2069353696
- Cited by
- 93
- References
- 17
- Citations by year
- 2023: 2 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 5 · 2017: 4 · 2016: 6 · 2015: 9 · 2014: 7 · 2013: 7 · 2012: 5
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- global cerebral ischemia, basilar artery occlusion, bilateral common carotid artery occlusion, C57BL/6 mice, anoxic depolarization, ischemic neuronal injury, ischemic time, genetic background effects, mouse strain differences
- MeSH terms
- Animals, Basilar Artery, Body Temperature, Brain Ischemia, Cerebrovascular Circulation, Disease Models, Animal, Electrophysiology, Hemodynamics, Hippocampus, Male, Mice, Inbred C57BL, Neurons, Regional Blood Flow, Surgical Instruments, In Situ Nick-End Labeling, Mice
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