PMID- 10401636
OWN - NLM
STAT- MEDLINE
DCOM- 19991019
LR  - 20141120
IS  - 1050-9631 (Print)
IS  - 1050-9631 (Linking)
VI  - 9
IP  - 3
DP  - 1999
TI  - Hypoxia-induced loss of synaptic transmission is exacerbated in hippocampal 
      slices of transgenic mice expressing C-terminal fragments of Alzheimer amyloid 
      precursor protein.
PG  - 201-5
AB  - To investigate the possible involvement of beta-amyloid (A beta) in disrupting 
      neuronal function during ischemia, we examined whether overexpression of 
      C-terminal fragments of beta-amyloid precursor protein (beta-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 CA1 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.
FAU - Ghribi, O
AU  - Ghribi O
AD  - Departement de Chimie-Biologie, Universite du Quebec, Canada.
FAU - Lapierre, L
AU  - Lapierre L
FAU - Girard, M
AU  - Girard M
FAU - Ohayon, M
AU  - Ohayon M
FAU - Nalbantoglu, J
AU  - Nalbantoglu J
FAU - Massicotte, G
AU  - Massicotte G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hippocampus
JT  - Hippocampus
JID - 9108167
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, Glutamate)
SB  - IM
MH  - Amyloid beta-Protein Precursor/*biosynthesis/chemistry
MH  - Animals
MH  - Excitatory Postsynaptic Potentials
MH  - Hippocampus/pathology/*physiopathology
MH  - Hypoxia, Brain/pathology/*physiopathology
MH  - In Vitro Techniques
MH  - Mice
MH  - Mice, Transgenic
MH  - Neurons/pathology/physiology
MH  - Peptide Fragments/*biosynthesis
MH  - Receptors, Glutamate/metabolism
MH  - Synaptic Transmission/*physiology
EDAT- 1999/07/13 00:00
MHDA- 1999/07/13 00:01
CRDT- 1999/07/13 00:00
PHST- 1999/07/13 00:00 [pubmed]
PHST- 1999/07/13 00:01 [medline]
PHST- 1999/07/13 00:00 [entrez]
AID - 10.1002/(SICI)1098-1063(1999)9:3<201::AID-HIPO1>3.0.CO;2-P [doi]
PST - ppublish
SO  - Hippocampus. 1999;9(3):201-5. doi: 
      10.1002/(SICI)1098-1063(1999)9:3<201::AID-HIPO1>3.0.CO;2-P.