Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as "continuum" phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrain.

@article{Northington2007FailureTC,
  title={Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as "continuum" phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrain.},
  author={Frances J. Northington and Mario Enrique Zelaya and D P O'riordan and Klas Blomgren and Debra L Flock and Henrik H Hagberg and D M Ferriero and Lee J. Martin},
  journal={Neuroscience},
  year={2007},
  volume={149 4},
  pages={822-33}
}
Controversy surrounds proper classification of neurodegeneration occurring acutely following neonatal hypoxia-ischemia (HI). By ultrastructural classification, in the first 24 h after neonatal hypoxia-ischemia in the 7-day-old (p7) rat, the majority of striatal cells die having both apoptotic and necrotic features. There is formation of a functional apoptosome, and activation of caspases-9 and -3 occurring simultaneously with loss of structurally intact mitochondria to 34.7+/-25% and loss of… CONTINUE READING

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