In vivo calcium imaging of cerebral cortex in hypoxia-ischemia followed by developmental stage-specific injury in rats.

The parietal area is a part of the cortex that is vulnerable in the rat to hypoxia-ischemia (HI) within the early postnatal period. To investigate the localizing mechanism of this cortical injury, we spatiotemporally detected the cortical intracellular calcium changes, as revealed by a calcium-sensitive fluorescence dye, Rhod 2-AM, during 1h of HI on postnatal days 7-21 in vivo. The calcium level rose to different levels at different cortical points in all animals within the first 20 min.

Cerebral hypoxia-ischemia in immature rats: involvement of mitochondrial permeability transition?

The aim of this study was to evaluate the involvement of mitochondrial membrane permeability transition (MPT) after hypoxia-ischemia (HI) in 7-day-old rats. [14C]2-deoxyglucose (DOG) was administered to controls, and at various time points after HI. MPT in the cerebral cortex was measured as entrapment of DOG-6-P in mitochondria.

Alterations in glutathione and amino acid concentrations after hypoxia-ischemia in the immature rat brain.

Hypoxic-ischemic brain injury involves an increased formation of reactive oxygen species. Key factors in the cellular protection against such agents are the GSH-associated reactions. In the present study we examined alterations in total glutathione and GSSG concentrations in mitochondria-enriched fractions and tissue homogenates from the cerebral cortex of 7-day-old rats at 0, 1, 3, 8, 14, 24 and 72 h after hypoxia-ischemia.

Impairment of mitochondrial respiration after cerebral hypoxia-ischemia in immature rats: relationship to activation of caspase-3 and neuronal injury.

Mitochondrial damage may play a key role in the development of necrotic and apoptotic hypoxic-ischemic (HI) brain damage. It has previously been shown that mitochondrial respiration is depressed in the cerebral cortex after HI in neonatal animals. The aim of the present study was to further characterize the time course of the mitochondrial impairment during reperfusion and the correlation between the respiratory control ratio and brain injury and activation of caspase-3.

Subcellular distribution of calcium and ultrastructural changes after cerebral hypoxia-ischemia in immature rats.

Recent data imply that mitochondrial regulation of calcium is critical in the process leading to hypoxic-ischemic brain injury. The aim was to study the subcellular distribution of calcium in correlation with ultrastructural changes after hypoxia-ischemia in neonatal rats. Seven-day-old rats were subjected to permanent unilateral carotid artery ligation and exposure to hypoxia (7.