Abstract
Considerable evidence has linked hydroxyl radicals ( · OH ) to excitotoxicity. Glutamate infused through a microdialysis probe into rat striatum induced a massive · OH production, which was completely blocked by PBN and attenuated by dizocilpine, 2-amino-5-phosphonopentanoic acid (AP-5), N G-nitro- l-arginine methyl ester ( l-NAME) and mepacrine. Thus, we suggest that the neurotoxic effects of glutamate in vivo may derive from an increased formation of · OH resulting from excessive activation of NMDA receptors and downstream enzymes such as NOS and PLA 2.
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