Glutamate (glu), an excitatory aminoacid neurotransmitter is abundantly present in the brain of mammals, as well as in dietary protein. Earlier studies with glu mostly involved histopathological and neuroendocrine changes in the blood-brain-barrier deficient areas of brain following its systemic administration. The present study examined lipid peroxidation potential and anti-oxidant parameters of immature rat mid-brain region which include arcuate nucleus, hypothalamus, and other circumventricular organs (CVO) following their exposure to monosodium glutamate (MSG) neonatally. This compound was administered at a dose of 4 mg/g bwt, sc, for the first ten days of postnatal period. Animals were sacrificed on postnatal day 25, and the lipid peroxidation potential was evaluated. The treatment of MSG significantly increased lipid peroxidation (P < 0.01) as well as the activity of anti-oxidant enzyme catalase (P < 0.025) and significantly depleted total and free sulfhydryl groups (P < 0.05) in the CVO. These results indicate that neonatal MSG treatment produces neuronal damage in the CVO by increasing lipid peroxidation and is in agreement with the hypothesis that excitotoxins may generate free radicals in causing neurotoxicity.