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Synaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice.

Authors
Veinbergs, I; Mante, M; Jung, MW; Van Uden, E; Masliah, E
Citation
Progress in neuro-psychopharmacology & biological psychiatry, 23(3):519-531, 1999
Journal Title
Progress in neuro-psychopharmacology & biological psychiatry
ISSN
0278-58461878-4216
Abstract
1. Aged apoE-deficient mice and age-matched controls were tested for cognitive alterations in the Morris water maze. 2. Water maze results were correlated with in vivo electrophysiology and expression of the synaptic protein synaptotagmin (p65). 3. Compared to age-matched controls, apolipoprotein E-deficient mice displayed significant performance impairment accompanied by in vivo electrophysiological alterations in the dentate gyrus. 4. Apolipoprotein E-deficient mice also showed a significant increase in the synaptic protein, synaptotagmin, a synaptic calcium sensor involved in neurotransmitter release. 5. Cognitive impairments in these animals may be associated with decreased synaptic excitability in hippocampal neurons and the regulatory role of apolipoprotein E in synaptic function might be mediated by modulation of the expression of calcium sensor proteins.
MeSH terms
Aging/physiology*Alzheimer Disease/physiopathologyAnimalsApolipoproteins E/deficiency*Calcium-Binding Proteins*Cognition Disorders/physiopathology*Dentate Gyrus/physiopathologyFemaleMaleMaze LearningMembrane Glycoproteins/pharmacology*MiceNerve Tissue Proteins/pharmacology*Synaptic Transmission/physiology*Synaptotagmin ISynaptotagmins
PMID
10378234
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
정, 민환
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