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Oxygen/glucose deprivation and reperfusion cause modifications of postsynaptic morphology and activity in the ca3 area of organotypic hippocampal slice cultures

Title
Oxygen/glucose deprivation and reperfusion cause modifications of postsynaptic morphology and activity in the ca3 area of organotypic hippocampal slice cultures
Authors
Jung Y.J.Suh E.C.Lee K.E.
Ewha Authors
이경은정연주
SCOPUS Author ID
이경은scopus; 정연주scopus
Issue Date
2012
Journal Title
Korean Journal of Physiology and Pharmacology
ISSN
1226-4512JCR Link
Citation
vol. 16, no. 6, pp. 423 - 429
Indexed
SCIE; SCOPUS; KCI WOS scopus
Abstract
Brain ischemia leads to overstimulation of N-methyl-D-aspartate (NMDA) receptors, referred as excitotoxicity, which mediates neuronal cell death. However, less attention has been paid to changes in synaptic activity and morphology that could have an important impact on cell function and survival following ischemic insult. In this study, we investigated the effects of reperfusion after oxygen/glucose deprivation (OGD) not only upon neuronal cell death, but also on ultrastructural and biochemical characteristics of postsynaptic density (PSD) protein, in the stratum lucidum of the CA3 area in organotypic hippocampal slice cultures. After OGD/reperfusion, neurons were found to be damaged; the organelles such as mitochondria, endoplasmic reticulum, dendrites, and synaptic terminals were swollen; and the PSD became thicker and irregular. Ethanolic phosphotungstic acid staining showed that the density of PSD was significantly decreased, and the thickness and length of the PSD were significantly increased in the OGD/reperfusion group compared to the control. The levels of PSD proteins, including PSD-95, NMDA receptor 1, NMDA receptor 2B, and calcium/calmodulin-dependent protein kinase II, were significantly decreased following OGD/reperfusion. These results suggest that OGD/reperfusion induces significant modifications to PSDs in the CA3 area of organotypic hippocampal slice cultures, both morphologically and biochemically, and this may contribute to neuronal cell death and synaptic dysfunction after OGD/reperfusion.
DOI
10.4196/kjpp.2012.16.6.423
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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