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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
vol. 29, no. 4, pp. 691 - 699
Indexed
SCI; SCIE; SCOPUS WOS scopus
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:
의학전문대학원 > 의학과 > Journal papers
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