## Abstract Excessive release of glutamate during transient cerebral ischemia initiates a cascade of events that leads to the delayed and selective death of neurons located in the hippocampus. Activity of calcium calmodulin kinase II (CaM kinase), a protein kinase critical to neuronal functioning,
Alterations of Calcium/Calmodulin-Dependent Protein Kinase II Activity in Ischaemia-Induced Neuronal Death and Neuronal Protection Against Ischaemia in the Gerbil Hippocampus
โ Scribed by H. Uno; H. Kobayashi; Y. Handa; M. Kabuto; T. Kubota
- Publisher
- Springer Vienna
- Year
- 1999
- Tongue
- English
- Weight
- 232 KB
- Volume
- 141
- Category
- Article
- ISSN
- 0001-6268
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## Abstract Delayed neuronal cell death occurs in the vulnerable CA1 subfield of the hippocampus after transient global ischemia (TGI). We demonstrated previously, based on an experimental model of TGI, that the significantly increased content of oxidized proteins in hippocampal CA1 neuron was obse