Ontogeny of excitotoxic injury to nicotinamide adenine dinucleotide phosphate diaphorase reactive neurons in the neonatal rat striatum.

To further define the ontogeny of "excitotoxic" injury to brain, intrastriatal injection of an N-methyl-D-aspartate agonist (quinolinate) and a non-N-methyl-D-aspartate agonist (quisqualate) was performed in rats at postnatal days 7 and 14, and in adults. Excitotoxic injury was quantified volumetrically and with neuronal counts of nicotine adenine dinucleotide phosphate-containing neurons as this cell population is spared in neonatal hypoxia ischemia. Only postnatal day 7 pups injected with quinolinic acid showed selective sparing of neurons containing the enzyme nicotinamide adenine dinucleotide phosphate. At postnatal day 14 and later ages, nicotinamide adenine dinucleotide phosphate neurons were susceptible to the actions of both quinolinic and quisqualic acids. The unusual sparing of nicotinamide adenine dinucleotide phosphate-reactive neurons after N-methyl-D-aspartate receptor agonist exposure in the first week of life appears to be unique to the neonatal brain and may be related to the pathophysiology of neonatal hypoxia-ischemia.