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Hypoxia‐Induced Loss of Synaptic Transmission Is Exacerbated in Hippocampal Slices of Transgenic Mice Expressing C‐Terminal Fragments of Alzheimer Amyloid Precursor Protein
Author(s) -
Ghribi Othman,
Lapierre Luc,
Girard Martine,
Ohayon Maurice,
Nalbantoglu Josephine,
Massicotte Guy
Publication year - 1999
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/(sici)1098-1063(1999)9:3<201::aid-hipo1>3.0.co;2-p
Subject(s) - hippocampal formation , neurotransmission , hippocampus , neuroscience , genetically modified mouse , glutamate receptor , hypoxia (environmental) , chemistry , amyloid precursor protein , transgene , microbiology and biotechnology , receptor , biophysics , medicine , biology , alzheimer's disease , biochemistry , disease , organic chemistry , oxygen , gene
To investigate the possible involvement of β‐amyloid (Aβ) in disrupting neuronal function during ischemia, we examined whether overexpression of C‐terminal fragments of β‐amyloid precursor protein (β‐APP) in transgenic (Tg) mice is capable of altering the capacity of hippocampus slices to recover synaptic transmission after transient hypoxic episodes. Recovery of synaptic transmission was monitored in area CA 1 of perfused hippocampal slices prepared from both control and Tg mice. The results obtained indicate that hippocampal slices prepared from Tg mice exhibited a much lower level of recovery in synaptic transmission following reoxygenation. This reduction in the capacity of Tg slices to recover from hypoxia‐induced impairment of synaptic transmission in the hippocampus does not appear to be related to pre‐existing alterations in either functional or biochemical properties of glutamate receptors in Tg mice. The present results provide the first experimental evidence that overexpression of the C‐terminal fragment of APP exacerbates functional damage of hippocampal neurons after hypoxic episodes. Hippocampus 1999;9:201–205. © 1999 Wiley‐Liss, Inc.