Hypoxia-Induced Loss of Synaptic Transmission Is Exacerbated in Hippocampal Slices of Transgenic Mice Expressing C-Terminal Fragments of Alzheimer Amyloid Precursor Protein
✍ Scribed by Othman Ghribi; Luc Lapierre; Martine Girard; Maurice Ohayon; Josephine Nalbantoglu; Guy Massicotte
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 128 KB
- Volume
- 9
- Category
- Article
- ISSN
- 1050-9631
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✦ Synopsis
To investigate the possible involvement of -amyloid (A) in disrupting neuronal function during ischemia, we examined whether overexpression of C-terminal fragments of -amyloid precursor protein (-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.