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Modification of postsynaptic densities after transient cerebral ischemia: a quantitative and three-dimensional
M E Martone1, Y Z Jones, S J Young
1Department of Neurosciences, National Center for Microscopy and Imaging Research at San Diego, University of California, San Diego, La Jolla, California 92093, USA.
Summary
Transient cerebral ischemia significantly alters synapses in the rat hippocampus. Postsynaptic densities (PSDs) become thicker and more irregular, potentially leading to neuronal death via calcium influx.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Abnormal synaptic transmission is a suspected cause of neuronal death after transient ischemia.
- The precise mechanisms underlying ischemia-induced neuronal damage remain incompletely understood.
Purpose of the Study:
- To investigate synaptic modifications in the hippocampus following transient cerebral ischemia.
- To elucidate the ultrastructural changes in postsynaptic densities (PSDs) after ischemic events.
Main Methods:
- Utilized conventional and high-voltage electron microscopy for two- and three-dimensional synaptic analysis.
- Employed ethanolic phosphotungstic acid staining for selective PSD visualization in rat hippocampus.
- Conducted quantitative analysis of PSD morphology over time during reperfusion periods.
Main Results:
- Postsynaptic densities (PSDs) in the hippocampus showed significant thickening and a 'fluffier' appearance post-ischemia.
- Three-dimensional electron tomography revealed more irregular and loosely configured PSDs in ischemic brains.
- Morphological changes in PSDs were more pronounced and persistent in the CA1 area compared to the dentate gyrus.
Conclusions:
- Degenerative ultrastructural alterations of PSDs may contribute to post-ischemic neuronal damage.
- Altered PSDs might generate toxic signals, such as increased calcium influx, leading to neuronal injury.
- These findings highlight synaptic PSDs as critical targets in understanding and potentially treating ischemic brain injury.