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Aβ25-35 induces presynaptic changes in organotypic hippocampal slice cultures

Title
Aβ25-35 induces presynaptic changes in organotypic hippocampal slice cultures
Authors
Suh E.C.Jung Y.J.Kim Y.A.Park E.M.Lee K.E.
Ewha Authors
이경은박은미
SCOPUS Author ID
이경은scopus; 박은미scopus
Issue Date
2008
Journal Title
NeuroToxicology
ISSN
0161-813XJCR Link
Citation
NeuroToxicology vol. 29, no. 4, pp. 691 - 699
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Memory loss in Alzheimer's disease (AD) may be related to synaptic defects in damaged hippocampal neurons. We investigated the relationship between amyloid peptide Aβ25-35-induced neuronal death pattern and presynaptic changes in organotypic hippocampal slice cultures. In propidium iodide (PI) uptake and annexin V labeling, Aβ25-35-induced neuronal damage dramatically increased in a concentration dependent manner, indicating both types of cell death. In ultrastructural analysis, apoptotic features in CA1 and CA3 area and synaptic disruption in stratum lucidum were detected in Aβ25-35-treated slices. Immunofluorescence and Western blot analysis for caspase-3 showed Aβ25-35 concentration dependently induced caspase-3 activation. Immunofluorescence and Western blot analysis to determine changes in presynaptic marker proteins demonstrated that expression of synaptosomal-associated protein-25 (SNAP-25) and synaptophysin were reduced by Aβ25-35 in CA1, CA3 and DG area at concentrations >2.5 μM. In conclusion, Aβ25-35-induced apoptotic cell death and caspase-3 activation at relatively low concentration, and induced synaptic disruption and loss of synaptic marker protein at concentrations >2.5 μM in organotypic hippocampal slice cultures. These suggest that Aβ25-35-induced apoptosis via triggering caspase-3 activation and lead to synaptic dysfunction in organotypic hippocampal slice cultures. © 2008 Elsevier Inc. All rights reserved.
DOI
10.1016/j.neuro.2008.04.001
Appears in Collections:
의과대학 > 의학과 > Journal papers
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