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Neurochem Res. 2008 Sep;33(9):1894-900. doi: 10.1007/s11064-008-9664-2. Epub 2008 Mar 25.

Mitochondria are more resistant to hypoxic depolarization in the newborn than in the adult brain.

Author information

1
Faculty Division Rikshospitalet, Institute for Surgical Research and Department of Neurosurgery, University of Oslo, Oslo, 0027, Norway.

Abstract

Hypoxic-ischemic brain injury subsequent to asphyxia represents a major cause of morbidity and death in the newborn. The newborn brain has been considered more resistant to hypoxia than the adult brain because of lower energy demand. The mechanisms underlying hypoxic brain injury, in particular the age-related vulnerability, are still only partially understood. The mitochondrial function is pivotal for the function and survival of neurons. Acutely isolated CA1 neurons from neonatal (3-6 days) and adult rats (5-6 weeks) were loaded with Rh 123, and the effect of hypoxia on the inner mitochondrial membrane potential (Delta psi(m)) was compared. During prolonged hypoxia (15 min), Delta psi(m) was lost in a majority of the neonatal neurons (83%) and in all the adult neurons. During hypoxia (5 min) followed by reoxygenation the mitochondria in 23% of the neonatal neurons were completely depolarized, whereas 85% of the adult neurons demonstrated a complete loss of Delta psi(m). In conclusion hippocampal CA1 mitochondria in the newborn rat are more resistant to hypoxic depolarization than in the adult rat.

PMID:
18363097
DOI:
10.1007/s11064-008-9664-2
[Indexed for MEDLINE]

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