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Calcium overload in selectively vulnerable neurons of the hippocampus during and after ischemia: an electron
Insights
Forebrain ischemia causes cell damage in rat hippocampus, particularly after reperfusion. Excessive calcium accumulation in mitochondria is linked to neuronal death in vulnerable cells.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Forebrain ischemia induces significant cytopathological changes.
- Understanding the role of calcium in neuronal damage is crucial.
Purpose of the Study:
- To investigate cytopathological changes in the rat hippocampus following ischemia and reperfusion.
- To determine the fine structural localization of calcium during these processes.
Main Methods:
- Light and electron microscopy were employed.
- The oxalate/pyroantimonate procedure was used for calcium localization.
Main Results:
- Ischemic cell changes, including mitochondrial swelling and astrocytic process swelling, were most prominent after 30 minutes of reperfusion.
- Dense calcium deposits were observed in swollen mitochondria of neurons at 30 minutes of reperfusion.
- After 120 minutes of reperfusion, most cells showed recovery, but vulnerable neurons exhibited condensation and vacuoles with calcium deposits.
Conclusions:
- Excessive calcium entry and mitochondrial calcium overload during reperfusion contribute to the death of selectively vulnerable neurons.
- The findings highlight the critical role of calcium homeostasis in neuronal survival after ischemic events.
Abstract:
Light and electron microscopy has been used to study the cytopathological changes in the rat hippocampus directly after a 30-min period of forebrain ischemia and after 30 or 120 min of reperfusion. The fine structural localization of calcium has been demonstrated using the oxalate/pyroantimonate procedure. Cellular changes considered typical of ischemia (swelling of astrocytic processes, distention of mitochondria, condensation of cytoplasm, "ischemic cell change") are most prominent after 30 min of reperfusion. At this time, dense calcium pyroantimonate deposits are evident in swollen mitochondria in pyramidal and hilar neurons. After 120 min of reperfusion, substantial restitution has occurred; most mitochondria appear normal and there are few calcium deposits. However, a small number of selectively vulnerable neurons (hilar and pyramidal neurons) show dense condensation (ischemic cell change) with multiple vacuoles containing calcium deposits. The role of excessive calcium entry and mitochondrial calcium overload during the reperfusion period in determining the death of selectively vulnerable neurons is discussed.