Age-related impairment of synaptic transmission but normal potentiation in transgenic mice that overexpress the human APP695SWE mutant form of amyloid precursor protein

Journal of Neuroscience

Volumn 21, Issue 13, 2001, Pages 4691-4698

  Fitzjohn, Stephen M ^a,d   Morton, Robin A ^a,b,c,e   Kuenzi, Frederick ^a,c   Rosahl, Thomas W ^c   Shearman, Mark ^c   Lewis, Huw ^c   Smith, David ^c   Reynolds, David S ^c   Davies, Ceri H ^b,f   Collingridge, Graham L ^a   Seabrook, Guy R ^c  

^a UNIVERSITY OF BRISTOL   (United Kingdom)

^b UNIVERSITY OF EDINBURGH   (United Kingdom)

^c NEUROSCIENCE RESEARCH CENTRE   (United Kingdom)

^d UNIVERSITY OF BRISTOL   (United Kingdom)

^e Novartis Inst for Medical Sciences   (United Kingdom)

^f GLAXOSMITHKLINE   (United Kingdom)

Author keywords

Alzheimer's disease; APP; Hippocampus; LTP; Synaptic plasticity; Transgenic

Indexed keywords

AMYLOID PRECURSOR PROTEIN; EXCITOTOXIN; KYNURENIC ACID;

AGING; ALZHEIMER DISEASE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN SLICE; COGNITIVE DEFECT; CONTROLLED STUDY; DENTATE GYRUS; ELECTROPHYSIOLOGY; FACILITATION; GENE OVEREXPRESSION; HIPPOCAMPUS; LONG TERM POTENTIATION; MOUSE; NERVE CELL PLASTICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SENILE PLAQUE; SYNAPSE; SYNAPTIC TRANSMISSION; TRANSGENIC MOUSE;

EID: 0035399822     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.21-13-04691.2001     Document Type: Article

References (41)

1. A data acquisition program for on-line analysis of long-term potentiation and long-term depression
2. Familial Alzheimer's disease-linked presenilin 1 variants elevate Aβ1-42/1-40 ratio in vitro and in vivo
3. Abnormal synaptic transmission in aged APP transgenic mice
4. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice
5. Cerebral hypoxia: Some new approaches and unanswered questions
6. Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production
7. Glutamatergic neurotransmission in Alzheimer's disease
8. Age-related cognitive deficits, impaired long-term potentiation and reduction in synaptic marker density in mice lacking the β-amyloid precursor protein
9. A receptors
10. sw transgenic mice
11. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein
12. Hypoxia-induced loss of synaptic transmission is exacerbated in hippocampal slices of transgenic mice expressing C-terminal fragments of Alzheimer's amyloid precursor protein
13. In vivo synaptic transmission in young and aged amyloid precursor protein transgenic mice
14. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease
15. Amyloid, the presenilins and Alzheimer's disease
16. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models
17. Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins
18. Correlative memory deficits, Aβ elevation and amyloid plaques in transgenic mice
19. sw transgenic mice develop age-related Aβ deposits and neuropil abnormalities, but no neuronal loss in CA1
20. Carboxyl-terminal fragment of Alzheimer's APP destabilizes calcium homeostasis and renders neuronal cells vulnerable to excitotoxicity
21. Beta-amyloid protein enhances macrophage production of oxygen free radicals and glutamate
22. The rd mutation in cGMP PDE-IV does not affect synaptic plasticity in mouse hippocampus
23. Alterations in synaptic transmission and long-term potentiation in hippocampal slices from young and aged PDAPP mice
24. Glutamate transporter alterations in Alzheimer disease are possibly associated with abnormal APP expression
25. The early events of oxygen and glucose deprivation: Setting the scene for neuronal death?
26. Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the beta-amyloid precursor protein
27. Presenilin-1 mutation increases neuronal vulnerability to focal ischemia in vivo and to hypoxia and glucose deprivation in cell culture: Involvement of perturbed calcium homeostasis
28. Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease
29. Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in the brain
30. Selective disruption of late-phase LTP in mice under-expressing presenilin-1
31. Impaired learning and LTP in mice expressing the carboxy terminus of the Alzheimer amyloid precursor protein
32. Alzheimer's disease: A re-examination of the amyloid hypothesis
33. Synaptic transmission and hippocampal long-term potentiation in transgenic mice expressing FAD-linked presenilin 1
34. Mutant genes in familial Alzheimer's disease and transgenic models
35. Transgenic animals relevant to Alzheimer's disease
36. Mechanisms contributing to the deficits in hippocampal synaptic plasticity in mice lacking amyloid precursor protein
37. Amyloid precursor proteins inhibit heme oxygenase activity and augment neurotoxicity in Alzheimer's disease
38. The mouse gene retinal degeneration (rd) may reduce the number of neurons present in the adult hippocampal dentate gyrus
39. Alzheimer's amyloid-beta peptide inhibits sodium/calcium exchange measured in rat and human brain plasma membrane vesicles
40. Enhanced synaptic potentiation in transgenic mice expressing presenilin 1 familial Alzheimer's disease is normalized with a benzodiazepine
41. Increased susceptibility to ischemic brain damage in transgenic mice overexpressing the amyloid precursor protein