Ascorbic acid protects neurons from injury induced by glutamate and NMDA.
We have previously shown that redox phenomena regulate the function of the NMDA receptor in the brain and that ascorbic acid (AA) behaves as a receptor antagonist. Here we examined the potential neuroprotective effects of AA against toxicity induced by NMDA and glutamate in rat cerebral cortical neurones in cultures. AA completely protected against injury induced by 100 microM NMDA and markedly reduced cell death induced by 500 microM NMDA or 50 microM glutamate. Dehydroascorbic acid (DHAA) did not provide significant neuroprotection. Hence, we propose that AA may serve in the CNS as a neuroprotectant.
Majewska
M D
MD
Neuropharmacology Laboratory, Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224.
Bell
J A
JA
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects; D003683:Dehydroascorbic Acid / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists; D005260:Female; D005971:Glutamates / Q000633:toxicity; D018698:Glutamic Acid; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors* / Q000633:toxicity; D009474:Neurons / Q000187:drug effects*; D010084:Oxidation-Reduction; D011247:Pregnancy; D051381:Rats
D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D018698:Glutamic Acid; D016202:N-Methylaspartate; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid