EXCITATORY AMINO ACIDS AND LEAD-INDUCED NEUROTOXICITY
نویسندگان
چکیده
منابع مشابه
Excitatory Amino Acids Interaction and Neurotoxicity
It is supposed that Glu, and OXY are synthesized and stored in the same structure and parts of the brain. Both Glu and its receptors are located in different neurosecretory nuclei of the hypothalamus which are associated with neuroendocrine function. It have been demonstrated the presence of Glu in nucleus Paraventricularis (PVN), nucleus Ventro-Medianus (VMN), nucleus arcuatus, nucleus Supraop...
متن کاملSpeculations on disease states induced by excitatory amino acids.
There is much current interest in excitatory amino acids and their receptors because of their postulated involvement in several disorders of the nervous system. They function as neurotransmitters, but can act as neurotoxins in some situations. They have been implicated in the pathogenesis of cerebral hypoxic/ischemic and hypoglycemic damage, in epilepsy, in some degenerative diseases, and in so...
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SIR: Recently, Klockgether and Turski proposed that antagonists of excitatory amino acids may be beneficial in the treatment of Parkinson's disease 1. This suggestion , previously put torward by others 2-4, is supported by recent findings of animal experiments as weil as by clinical data. On the basis of these findings, a somewhat different conclusion can be drawn about the role of gluta-mate i...
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Excitatory amino acids (EAA) such as glutamate and aspartate are major transmitters of the cerebral cortex and hippocampus, and EAA mechanisms appear to play a role in learning and memory. Anatomical and biochemical evidence suggests that there is both pre- and postsynaptic disruption of EAA pathways in Alzheimer's disease. Dysfunction of EAA pathways could play a role in the clinical manifesta...
متن کاملThe neurotoxicity of excitatory amino acids is produced by passive chloride influx.
In the 15 years since the neurotoxic properties of glutamate and related amino acids were first described, there has been no thoroughly convincing explanation of the pathophysiology of excitatory amino acid-induced neuronal death. These substances depolarize central neurons, increase the frequency of neuronal discharge, and augment synaptic activity, leading to the suggestion that one or more o...
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ژورنال
عنوان ژورنال: The Journal of Toxicological Sciences
سال: 1998
ISSN: 0388-1350,1880-3989
DOI: 10.2131/jts.23.supplementii_181