Nitric oxide (NO) may mediate some of the toxic effects of the excitat
ory amino acid (EAA) glutamate when there is overactivation of the N-m
ethyl-D-aspartate (NMDA) receptor. In the developing rodent nervous sy
stem, NMDA neurotoxicity peaks at postnatal day 7. To assess whether N
O toxicity exhibits a similar developmental profile, we injected the N
O generator sodium nitroprusside into the immature and adult rodent hi
ppocampal formation and striatum, using a dose known to damage the adu
lt nervous system. Contrary to our expectations, we found the immature
brain highly resistant to the toxic effects of sodium nitroprusside.