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Phospholipid metabolism and second messenger system after brain ischemia
1Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Advances in Experimental Medicine and Biology
|January 1, 1992
Summary
Brain cell damage after ischemia may involve phospholipid metabolism changes. Specifically, hippocampal CA1 neurons show impaired recovery of polyphosphoinositides (PPIs) and elevated arachidonic acid (AA), suggesting membrane damage and excitotoxicity.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Selective neuronal damage occurs in specific brain regions following ischemic events.
- Phospholipid metabolism and second messenger systems are implicated in cellular responses to ischemia.
Purpose of the Study:
- To investigate the role of phospholipid metabolism and second messenger systems in selective neuronal damage after transient ischemia.
- To compare changes in vulnerable (hippocampal CA1) and resistant (parietal cortex) brain areas.
Main Methods:
- Gerbil model of transient ischemia and reperfusion.
- Measurement of polyphosphoinositides (PPIs) and free fatty acids (FFAs).
- Autoradiographic analysis of protein kinase C (PKC) and IP3 receptor binding.
- Northern blot analysis for heat shock protein 70 (HSP70) and amyloid precursor protein (APP) mRNA.
Main Results:
- Vulnerable hippocampal CA1 neurons showed impaired recovery of PPIs and sustained elevation of arachidonic acid (AA) compared to resistant cortical areas.
- Decreased protein kinase C (PKC) binding and IP3 receptor binding were observed in CA1 cells post-reperfusion.
- HSP70 mRNA was induced, but APP mRNA was not; induction levels varied regionally, with less in CA1 cells.
- IP3 receptor binding decreased earlier than PKC binding or observable neuronal damage.
Conclusions:
- CA1 cell membranes may not fully recover after transient ischemia, with early alterations in endoplasmic reticulum membranes.
- Regional differences in HSP70 mRNA induction correlate with neuronal vulnerability.
- Inositol phospholipid metabolism, second messenger systems, and HSP70 induction may contribute to excitotoxic neuronal damage in the hippocampus.
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