The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Reversible impairment of long‐term potentiation in transgenic Cu/Zn‐SOD mice
Open accessAbstract
Copper/zinc superoxide dismutase (CuZn‐SOD) is a key enzyme in the metabolism of oxygen free radicals. The gene encoding CuZn‐SOD resides on human chromosome 21 and is overexpressed in Down syndrome (DS) patients. Overexpression of CuZn‐SOD in transgenic (Tg) mice and cultured cells creates chronic oxidative stress leading to enhanced susceptibility to degeneration and apoptotic cell death. We have now found that three lines of Tg‐CuZn‐SOD mice, one of which also overexpresses S100β, a glial calcium binding protein, are deficient in spatial memory. Furthermore, hippocampal slices taken from these mice have an apparently normal synaptic physiology, but are impaired in the ability to express long‐term potentiation (LTP). This effect on hippocampal LTP was abrogated by treatment of slices with the H 2 O 2 scavenger catalase or the antioxidant N‐t‐butyl‐phenylnitrone (BPN). It is proposed that elevated CuZnSOD causes an increase in tetanic stimulation‐evoked formation of H 2 O 2 which leads to diminished LTP and cognitive deficits in these mice.
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Cites
Reactive Oxygen Species and the Central Nervous System
Halliwell, B. (1992) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1992.tb10990.x · Cited by 2,947
Apoptosis and increased generation of reactive oxygen species in Down's syndrome neurons in vitro
Busciglio, J., & Yankner, B. A. (1995) · Nature · doi:10.1038/378776a0 · Cited by 741
A novel cholinergic induction of long-term potentiation in rat hippocampus
Auerbach, J. M., & Segal, M. (1994) · Journal of Neurophysiology · doi:10.1152/jn.1994.72.4.2034 · Cited by 166 · cited 4×
“Hippocampal slices were maintained in a submerged configuration and extracellular recording was performed from stratum radiatum of area CA1 of the slice (as in Auerbach & Segal, 1994).”
MethodInfluentialSelf-citation
Cited by
Halliwell, B. (2001) · Drugs & Aging · doi:10.2165/00002512-200118090-00004 · Cited by 1,502
Mitochondria, oxygen free radicals, disease and ageing
Raha, S., & Robinson, B. H. (2000) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(00)01674-1 · Cited by 1,066
Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory
Massaad, C. A., & Klann, E. (2011) · Antioxidants & Redox Signaling · doi:10.1089/ars.2010.3208 · Cited by 635
Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications
Lei, X. G., Zhu, J.-H., Cheng, W.-H., Bao, Y., Ho, Y.-S., Reddi, A. R., Holmgren, A., & Arnér, E. S. J. (2016) · Physiological Reviews · doi:10.1152/physrev.00010.2014 · Cited by 429
Beckhauser, T. F., Francis-Oliveira, J., & De Pasquale, R. (2016) · Journal of Experimental Neuroscience · doi:10.4137/jen.s39887 · Cited by 301
Metadata
- Authors
- Gahtan, E., Auerbach, J. M., Groner, Y., & Segal, M.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 1998-02
- Volume
- 10
- Issue
- 2
- Pages
- 538-544
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2063256334
- Cited by
- 163
- References
- 3
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Gahtan, E., Auerbach, J. M., Groner, Y., & Segal, M. (1998). Reversible impairment of long‐term potentiation in transgenic Cu/Zn‐SOD mice. European Journal of Neuroscience. https://doi.org/10.1046/j.1460-9568.1998.00058.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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