Synaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice

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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 B-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.
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Issue Date
1999-04
Language
English
Article Type
Review
Keywords

ALZHEIMERS-DISEASE; CHOLINERGIC IMPAIRMENTS; VESICLE PROTEIN; NEURODEGENERATION; INJURY; BRAIN; APOE

Citation

PROGRESS IN NEURO-PSYCHOPHARMACOLOGY BIOLOGICAL PSYCHIATRY, v.23, no.3, pp.519 - 531

ISSN
0278-5846
DOI
10.1016/S0278-5846(99)00013-5
URI
http://hdl.handle.net/10203/78155
Appears in Collection
BS-Journal Papers(저널논문)
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