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The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Age-Related Impairment of Synaptic Transmission But Normal Long-Term Potentiation in Transgenic Mice that Overexpress the Human APP695SWE Mutant Form of Amyloid Precursor Protein

Fitzjohn, Stephen M., Morton, Robin A., Kuenzi, Frederick, Rosahl, Thomas W., Shearman, Mark, Lewis, Huw, Smith, David, Reynolds, David S., Davies, Ceri H., Collingridge, Graham L., Seabrook, Guy R.·2001·The Journal of Neuroscience
DOI 10.1523/jneurosci.21-13-04691.2001
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Abstract

We have studied synaptic function in a transgenic mouse strain relevant to Alzheimer's disease (AD), overexpressing the 695 amino acid isoform of human amyloid precursor protein with K670N and M671L mutations (APP 695 SWE mice), which is associated with early-onset familial AD. Aged-transgenic mice had substantially elevated levels of Aβ (up to 22 μmol/gm) and displayed characteristic Aβ plaques. Hippocampal slices from 12-month-old APP 695 SWE transgenic animals displayed reduced levels of synaptic transmission in the CA1 region when compared with wild-type littermate controls. Inclusion of the ionotropic glutamate receptor antagonist kynurenate during preparation of brain slices abolished this deficit. At 18 months of age, a selective deficit in basal synaptic transmission was observed in the CA1 region despite treatment with kynurenate. Paired-pulse facilitation and long-term potentiation (LTP) were normal in APP 695 SWE transgenic mice at both 12 and 18 months of age. Thus, although aged APP 695 SWE transgenic mice have greatly elevated levels of Aβ protein, increased numbers of plaques, and reduced basal synaptic transmission, LTP can still be induced and expressed normally. We conclude that increased susceptibility to excitotoxicity rather than a specific effect on LTP is the primary cause of cognitive deficits in APP 695 SWE mice.

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  • Posttetanic potentiation and long-term potentiation in the CA1 area were apparently normal in Tg2576 hippocampal slices at both ages.

    “Note that posttetanic potentiation and LTP in the CA1 area were apparently normal in Tg2576 hippocampal slices at both ages, which is in agreement with previous reports that LTP was not impaired until at the age of >12 mo old (Chapman et al., 1999; Fitzjohn et al., 2001).”

    From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Fitzjohn et al., 2001

    The CA1 synaptic-plasticity results (page unavailable) report normal LTP in transgenic slices at both 12 and 18 months. The paper does not report posttetanic potentiation; it measures paired-pulse facilitation instead. Its finding of normal LTP at 18 months also does not support the sentence’s implication that LTP becomes impaired after 12 months. (LLM, conf=0.87)

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  • In the Schaffer collateral pathway (SC-CA1), the deficiency was not detectable until 12-18 months old.

    “In the Schaffer collateral (SC) pathway (SC-CA1), the deficiency was not detectable until 12–18 mo old (Chapman et al., 1999; Fitzjohn et al., 2001).”

    From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Fitzjohn et al., 2001

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Citations

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Research works printed but not linked: 35

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Metadata

Authors
Fitzjohn, S. M., Morton, R. A., Kuenzi, F., Rosahl, T. W., Shearman, M., Lewis, H., Smith, D., Reynolds, D. S., Davies, C. H., Collingridge, G. L., & Seabrook, G. R.
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
2001-07-01
Volume
21
Issue
13
Pages
4691-4698
ISSN
  • 0270-6474
  • 1529-2401
DOI
10.1523/jneurosci.21-13-04691.2001
Cited by
168
References
6
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)

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