Neuroprotective effects of graded reoxygenation following chronic hypoxia in neuronal cell cultures
Autor: | Phyllis K. Sher, Shuxian Hu |
---|---|
Rok vydání: | 1992 |
Předmět: |
medicine.medical_specialty
Partial Pressure Biology Models Biological Neuroprotection Mice chemistry.chemical_compound Fetus Glutamates Glutamate-Ammonia Ligase Lactate dehydrogenase Internal medicine medicine Animals Hypoxia Brain Cells Cultured gamma-Aminobutyric Acid Cerebral Cortex Neurons Hyperoxia Dose-Response Relationship Drug L-Lactate Dehydrogenase General Neuroscience Glutamate binding Hypoxia (medical) Receptors GABA-A Cell Hypoxia Receptors Neurotransmitter Surgery Oxygen medicine.anatomical_structure Endocrinology Receptors Glutamate chemistry Cerebral cortex Cell culture Room air distribution medicine.symptom |
Zdroj: | Neuroscience. 47:979-984 |
ISSN: | 0306-4522 |
DOI: | 10.1016/0306-4522(92)90045-4 |
Popis: | The present study was undertaken to investigate the comparative effects of rapid vs graded correction of chronic hypoxia in vitro. Cerebral cortical cell cultures obtained from fetal mice were exposed to 5% O2 for 24 h and returned immediately to room air for the following 24 h (Group I); comparable cultures were exposed to 5% O2 for 24 h followed by 10% O2 for an additional 24 h before return to room air (Group II). At the conclusion of the experimental protocol (time 0), partial pressure of oxygen in the bathing medium of Group I cultures was significantly higher than that of Group II and non-hypoxic controls (151 mmHg vs 124 and 132 mmHg, respectively; P less than 0.05). Throughout the recovery period, Group II cultures evidenced improved neuronal survival (e.g. 35,800 vs 17,700 neurons/culture well at time 0, P less than 0.01), decreased lactate dehydrogenase efflux into the bathing medium, relative preservation of neuronal morphology, as well as higher specific and clonazepam-displaceable benzodiazepine binding and GABA uptake. Glutamate binding was not differentially affected and glutamine synthetase activity, a predominantly glial marker, was only modestly increased after graded reoxygenation. These results demonstrate that gradual reoxygenation after prolonged hypoxia in vitro (i) improves neuronal survival compared to rapid reoxygenation and (ii) delays the manifestations of metabolic dysfunction even though the length of hypoxic exposure is increased. The findings are also consistent with the concept that a period of relative hyperoxia may contribute to hypoxia-induced neuronal injury. |
Databáze: | OpenAIRE |
Externí odkaz: |