salicylates and 3-5-dihydroxyphenylglycine

Hydroxyl radicals (.OH) are frequently associated with glutamate excitotoxicity and may be critical in the occurrence of perinatal brain damage. We thus investigated the mechanisms regulating the glutamate-induced release of toxic.OH during development, using microdialysis and salicylate as an.OH trap. Glutamate inhibited.OH release until post-natal day 14, but stimulated this release from day 21 onwards. DHPG [(RS)-3,5-dihydroxyphenylglycine], a group-I metabotropic glutamate receptor agonist, similarly reduced the.OH release at day 14, but was ineffective afterwards. DHPG also completely blunted the tremendous NMDA-induced.OH release at day 14 but not at day 21. Glutamate itself therefore tonically inhibited a possible free radical release through NMDA channel activation during early development.

Topics: Aging; Animals; Animals, Newborn; Brain; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Glutamic Acid; Glycine; Hydroxyl Radical; Microdialysis; N-Methylaspartate; Neurons; Neurotoxins; Oxidative Stress; Rats; Rats, Wistar; Receptors, Metabotropic Glutamate; Receptors, N-Methyl-D-Aspartate; Resorcinols; Salicylates