Upregulation of nitric oxide synthase II contributes to apoptotic cell death in the hippocampal CA3 subfield via a cytochrome c/caspase-3 signaling cascade following induction of experimental temporal lobe status epilepticus in the rat.

@article{Chuang2007UpregulationON,
  title={Upregulation of nitric oxide synthase II contributes to apoptotic cell death in the hippocampal CA3 subfield via a cytochrome c/caspase-3 signaling cascade following induction of experimental temporal lobe status epilepticus in the rat.},
  author={Yao Chi Chuang and San- Duo Chen and T. K. Lin and Chia Wei Liou and Wen-Neng Chang and Samuel H. H. Chan and Alice Y. W. Chang},
  journal={Neuropharmacology},
  year={2007},
  volume={52 5},
  pages={1263-73}
}
Status epilepticus results in preferential neuronal cell loss in the hippocampus. We evaluated the hypothesis that the repertoire of intracellular events in the vulnerable hippocampal CA3 subfield after induction of experimental temporal lobe status epilepticus entails upregulation of nitric oxide synthase II (NOS II), followed by the release of mitochondrial cytochrome c that triggers the cytosolic caspase-3 cascade, leading to apoptotic cell death. In Sprague-Dawley rats, significant and… CONTINUE READING
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