Adenosine reduces cortical neuronal injury induced by oxygen or glucose deprivation in vitro.
The endogenous neuromodulatory purine, adenosine, substantially attenuated neuronal degeneration when added to dissociated cortical cell cultures acutely deprived of either oxygen or glucose. The protective effect of adenosine, was concentration-dependent between 30 and 1000 microM (EC50 about 100 microM), and could be mimicked by the stable adenosine analogue N6-cyclohexyladenosine (10 microM). Unlike postsynaptic glutamate receptor antagonists, which also block these forms of neuronal injury, adenosine did not alter the neurotoxicity of exogenously applied glutamate.
Department of Neurology, Stanford University School of Medicine, CA 94305.
M P
MP
Goldberg
H
H
Monyer
J H
JH
Weiss
D W
DW
Choi
D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000201:enzymology / Q000473:pathology*; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000172:deficiency*; D000860:Hypoxia / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009474:Neurons / Q000201:enzymology / Q000473:pathology*; D009994:Osmolar Concentration
C027513:N(6)-cyclohexyladenosine; D007770:L-Lactate Dehydrogenase; D005947:Glucose; D000241:Adenosine