Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosis.

摘要: Brain injury in newborns can cause deficits motor and sensory function. In most models of neonatal brain injury, thalamic damage often occurs. Using the Rice-Vannucci model hypoxic-ischemic we have shown that neuronal degeneration somatosensory thalamus is delayed onset ( approximately 24 hr) compared with cortical striatal exhibits prominent structural features apoptosis. present study, examined whether cell death has molecular Fas receptor protein expression increased rapidly after hypoxia-ischemia, concert cleavage procaspase 8 to its active form. Concurrently, levels Bax mitochondrial-enriched fractions increase, cytochrome c accumulates soluble fraction. Mitochondria accumulate a perinuclear distribution by 6 hr hypoxia-ischemia. Cytochrome oxidase subunit 1 also increase at Increased receptor, Bax, c, activation caspase 8, abnormalities mitochondria significantly precede 3 appearance apoptosis hr. We conclude neurodegeneration rat ventral basal mediated activation.