The role of NO and B-50 in neurotoxicity of excitatory amino acids.

Abstract

To investigate the direct evidence for the role which nitric oxide (NO) plays in the neurotoxicity of excitatory amino acids, we evaluated NO level by Greiss testing solution when glutamate (Glu) and kainate (KA) induced neuronal degeneration in primary cortical cultures. Glutamate-induced neurotoxicity was accompanied by a rise in NO. 5 mM hemoglobin (Hb) led to a decrease of NO content and prevented excitotoxicity induced by 1 mM glutamate. 1 mM L-arginine (L-Arg) reversed the effect of hemoglobin by raising the NO level. No change in NO content was found in KA-induced neurotoxicity, which was not affected by L-Arg, Hb or L-Arg + Hb. It is suggested that NO plays an important role in glutamate-, but not KA-induced neurotoxicity in primary cortical cultures. We also investigated the effects of glutamate on a growth-associated protein, B-50. The B-50 level declined significantly 24 h after exposure to 100 microM glutamate for 30 min and then recovered 2 days later. The effect of glutamate on B-50 was concentration-dependent. This indicates that B-50 might be involved in both glutamate neurotoxicity and the following neuronal repair process.