Abstract: Forebrain ischemia in gerbils, produced by brief bilateral carotid occlusion, induced the dramatic loss of Ca2+/ calmodulin‐dependent protein kinase II (CaM‐kinase II) as determined by both kinase activity assays and western blot analysis. In cortex and hippocampus, cytosolic CaM‐kinase II was completely lost within 2–5 min of ischemia. Particulate CaM‐kinase II was more stable and decreased in level ~40% after 10 min of ischemia followed by 2 h of reperfusion. CaM‐kinase II in cerebellum, which does not become ischemic, was not affected. The rapid loss of CaM‐kinase II within 2‐5 min was quite specific because cytosolic cyclic AMP kinase and protein kinase C in hippocampus were not affected. These data indicate that cytosolic CaM‐kinase II is one of the most rapidly degraded proteins after brief ischemia. Because the multifunctional CaM‐kinase II has been implicated in the regulation of numerous neuronal functions, its loss may destine the neuronal cell for death.
|Number of pages||8|
|Journal||Journal of Neurochemistry|
|Publication status||Published - 1992 Mar|
- Neuronal cell death
- Protein kinase
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience