Hypoxic neuronal injury in vitro depends on extracellular glutamine.
Hypoxic neuronal injury (HNI) in cortical cell cultures was enhanced in a concentration-dependent fashion by the presence of 500 microM to 2 mM (EC50 about 500 microM) glutamine in the medium, concentrations approximating those normally present in cerebrospinal fluid (CSF). Regardless of the glutamine concentration, glutamate receptor antagonists 2-amino-5-phosphonovalerate or dextrorphan could substantially reduce HNI. Thus, the availability of extracellular glutamine could be a determinant of hypoxic neuronal injury in vivo, most likely reflecting its importance in the synthesis of the neurotransmitter excitotoxins glutamate and aspartate.
Goldberg
M P
MP
Department of Neurology, Stanford University School of Medicine, CA 94305.
Monyer
H
H
Choi
D W
DW
D000693:Anaerobiosis; D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000473:pathology*; D005333:Fetus; D005973:Glutamine / Q000494:pharmacology*; D000860:Hypoxia / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D051379:Mice; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000473:pathology*; D012016:Reference Values
D005973:Glutamine; D007770:L-Lactate Dehydrogenase