A study of long-term potentiation in transgenic mice over-expressing mutant forms of both amyloid precursor protein and presenilin-1.

Molecular Brain
Stephen M FitzjohnGraham L Collingridge

Abstract

Synaptic transmission and long-term potentiation (LTP) in the CA1 region of hippocampal slices have been studied during ageing of a double transgenic mouse strain relevant to early-onset familial Alzheimer's disease (AD). This strain, which over-expresses both the 695 amino acid isoform of human amyloid precursor protein (APP) with K670N and M671L mutations and presenilin 1 with the A246E mutation, has accelerated amyloidosis and plaque formation. There was a decrease in synaptic transmission in both wildtype and transgenic mice between 2 and 9 months of age. However, preparing slices from 14 month old animals in kynurenic acid (1 mM) counteracted this age-related deficit. Basal transmission and paired-pulse facilitation was similar between the two groups at all ages (2, 6, 9 and 14 months) tested. Similarly, at all ages LTP, induced either by theta burst stimulation or by multiple tetani, was normal. These data show that a prolonged, substantially elevated level of Abeta are not sufficient to cause deficits in the induction or expression of LTP in the CA1 hippocampal region.

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Citations

Aug 24, 2012·Molecular Neurobiology·Robert NisticòGraham Collingridge
Jun 13, 2012·Neuroscience·J PozuetaM L Shelanski
Jul 30, 2014·Life Sciences· NehaNirmal Singh
Feb 11, 2014·Behavioural Brain Research·John A Kennard, Fiona E Harrison
Feb 24, 2019·Acta Neuropathologica Communications·Sarmi SriMariana Vargas-Caballero

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Methods Mentioned

BETA
transgenic
PCR
time-resolved fluorescence
dissection
dissections

Software Mentioned

Excel 97 Toolpack
SPIKE
BMDP

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