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quisqualic acid/ischemia
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7 rezultātiem
Selective destruction of nitric oxide synthase neurons with quisqualate reduces damage after hypoxia-ischemia in the neonatal rat.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
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.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
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.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
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
Neuroprotective mechanism of (+)SKF 10,047 in vitro and in gerbil global brain ischemia.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
The N-methyl-D-aspartate receptor is believed to mediate part of the ischemic neuronal damage caused by the excitatory amino acid glutamate. (+)SKF 10,047, the prototypic sigma-agonist, interacts with the N-methyl-D-aspartate receptor. Therefore, we studied the neuroprotective effect of
Ontogeny of excitotoxic injury to nicotinamide adenine dinucleotide phosphate diaphorase reactive neurons in the neonatal rat striatum.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
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
The roads to mitochondrial dysfunction in a rat model of posttraumatic syringomyelia.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The pathophysiology of posttraumatic syringomyelia is incompletely understood. We examined whether local ischemia occurs after spinal cord injury. If so, whether it causes neuronal mitochondrial dysfunction and depletion, and subsequent energy metabolism impairment results in cell starvation of
4-(Tetrazolylalkyl)piperidine-2-carboxylic acids. Potent and selective N-methyl-D-aspartic acid receptor antagonists with a short duration of action.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
We have prepared a series of cis-4-(tetrazolylakyl)piperidine-2-carboxylic acids as potent and selective N-methyl-D-aspartic acid (NMDA) receptor antagonists. NMDA antagonists may prove to be useful therapeutic agents, for instance, as anticonvulsants, in the treatment of neurodegenerative disorders
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