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Titolo:
Age-related impairment of synaptic transmission but normal long-term potentiation in transgenic mice that overexpress the human APP695SWE mutant formof amyloid precursor protein
Autore:
Fitzjohn, SM; Morton, RA; Kuenzi, F; Rosahl, TW; Shearman, M; Lewis, H; Smith, D; Reynolds, DS; Davies, CH; Collingridge, GL; Seabrook, GR;
Indirizzi:
Univ Bristol, Sch Med Sci, Dept Anat, MRC,Ctr Synapt Plast, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England Univ Edinburgh, Dept Pharmacol, Edinburgh EH8 9JZ, Midlothian, Scotland Univ Edinburgh Edinburgh Midlothian Scotland EH8 9JZ Midlothian, Scotland Merck Sharp & Dohme Ltd, Neurosci Res Ctr, Res Labs, Harlow CM20 2QR, Essex, England Merck Sharp & Dohme Ltd Harlow Essex England CM20 2QR 2QR, Essex, England
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 13, volume: 21, anno: 2001,
pagine: 4691 - 4698
SICI:
0270-6474(20010701)21:13<4691:AIOSTB>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ALZHEIMERS-DISEASE; IN-VIVO; LINKED PRESENILIN-1; CALCIUM HOMEOSTASIS; GLUCOSE DEPRIVATION; HIPPOCAMPAL SLICES; MUTATION; DEFICITS; HYPOXIA; BRAIN;
Keywords:
Alzheimer's disease; synaptic plasticity; LTP; hippocampus; APP; transgenic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Fitzjohn, SM Univ Bristol, Sch Med Sci, Dept Anat, MRC,Ctr Synapt Plast, Univ Walk, Bristol BS8 1TD, Avon, England Univ Bristol Univ Walk Bristol Avon England BS8 1TD , England
Citazione:
S.M. Fitzjohn et al., "Age-related impairment of synaptic transmission but normal long-term potentiation in transgenic mice that overexpress the human APP695SWE mutant formof amyloid precursor protein", J NEUROSC, 21(13), 2001, pp. 4691-4698

Abstract

We have studied synaptic function in a transgenic mouse strain relevant toAlzheimer'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 micehad substantially elevated levels of A beta (up to 22 mu mol/gm) and displayed characteristic A beta 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 12and 18 months of age. Thus, although aged APP(695)SWE transgenic mice havegreatly elevated levels of A beta 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 07:40:48