Hypoxia-induced loss of synaptic transmission is exacerbated in hippocampal slices of transgenic mice expressing C-terminal fragments of Alzheimer amyloid precursor protein

Hippocampus

Volumn 9, Issue 3, 1999, Pages 201-205

  Ghribi, Othman ^a   Lapierre, Luc ^a   Girard, Martine ^a   Ohayon, Maurice ^c   Nalbantoglu, Josephine ^b   Massicotte, Guy ^a,c  

^a UNIVERSITÉ DU QUÉBEC À TROIS RIVIÈRES   (Canada)

^b MCGILL UNIVERSITY   (Canada)

^c Institut Philippe Pinel de Montreal   (Canada)

Author keywords

CA1 slices; Hippocampus; Ischemia; Mice; Transgenic

Indexed keywords

AMYLOID PRECURSOR PROTEIN; GLUTAMATE RECEPTOR;

ALZHEIMER DISEASE; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CARBOXY TERMINAL SEQUENCE; CELL DAMAGE; CONTROLLED STUDY; ELECTROPHYSIOLOGY; GENE OVEREXPRESSION; HIPPOCAMPUS; HUMAN TISSUE; HYPOXIA; MOUSE; NERVE FUNCTION; NONHUMAN; PRIORITY JOURNAL; REOXYGENATION; SYNAPTIC TRANSMISSION; TRANSGENIC MOUSE;

AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; EXCITATORY POSTSYNAPTIC POTENTIALS; HIPPOCAMPUS; HYPOXIA, BRAIN; MICE; MICE, TRANSGENIC; NEURONS; PEPTIDE FRAGMENTS; RECEPTORS, GLUTAMATE; SYNAPTIC TRANSMISSION;

EID: 0033012889     PISSN: 10509631     EISSN: None     Source Type: Journal    
DOI: 10.1002/(SICI)1098-1063(1999)9:3<201::AID-HIPO1>3.0.CO;2-P     Document Type: Article

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