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quisqualic acid/hypoxia
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Selective destruction of nitric oxide synthase neurons with quisqualate reduces damage after hypoxia-ischemia in the neonatal rat.
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The vulnerability of the developing CNS to hypoxia-ischemia (H-I) differs from that of the mature brain and is due in part to release of nitric oxide (NO) from parenchymal neurons. If NO is important in the generation of excitotoxic injury after H-I in the developing CNS, then selective destruction
Perinatal hypoxic-ischemic brain injury enhances quisqualic acid-stimulated phosphoinositide turnover.
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In an experimental model of perinatal hypoxic-ischemic brain injury, we examined quisqualic acid (Quis)-stimulated phosphoinositide (PPI) turnover in hippocampus and striatum. To produce a unilateral forebrain lesion in 7-day-old rat pups, the right carotid artery was ligated and animals were then
N-methyl-D-aspartate-mediated injury enhances quisqualic acid-stimulated phosphoinositide turnover in perinatal rats.
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Previous work in our laboratory demonstrated that ischemic-hypoxic brain injury in postnatal day 7 rats causes a substantial increase in phosphoinositide (PPI) turnover stimulated by the glutamate analogue quisqualic acid (QUIS) in the hippocampus and striatum. To examine this phenomenon in more
Effects of glutamate, quisqualate, and N-methyl-D-aspartate in neonatal brain.
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The intracerebral injection of the excitotoxins, glutamate (GLU), or its analogues, quisqualic acid (QA) and N-methyl-D-aspartate (NMDA), produces neuropathologic changes which resemble those induced by hypoxic-ischemic injury. We employed proton magnetic resonance spectroscopy to investigate the
Ontogeny of excitotoxic injury to nicotinamide adenine dinucleotide phosphate diaphorase reactive neurons in the neonatal rat striatum.
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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
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