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Journal ArticleDOI

Riluzole inhibits the release of glutamate in the caudate nucleus of the cat in vivo

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TLDR
When applied locally to the caudate nucleus of the halothane-anaesthetized cat, riluzole markedly reduced (-57%) the spontaneous release of glutamate, since the efflux of the other amino acids, including aspartate was not affected.
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This article is published in Neuroscience Letters.The article was published on 1992-12-07. It has received 157 citations till now. The article focuses on the topics: Riluzole & Glutamate receptor.

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Journal ArticleDOI

The role of excitotoxicity in neurodegenerative disease: implications for therapy.

TL;DR: There now seems to be little doubt that such a process is indeed a determining factor in the extent of the lesions observed, and direct evidence for a pathogenic role for excitotoxicity in neurological disease is missing.
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The pharmacology and mechanism of action of riluzole

A. Doble
- 01 Dec 1996 - 
TL;DR: In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemIA-evoked surge in glutamic acid release has been observed and it is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals.
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Melatonin, hydroxyl radical‐mediated oxidative damage, and aging: A hypothesis

TL;DR: Experiments investigating the effects of endogenous excitatory amino acid antagonists and stimulants of melatonin biosynthesis such as magnesium may finally lead to novel therapeutic approaches for the prevention of degeneration and dysdifferentiation associated with diseases related to premature aging.
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Replicating Huntington's disease phenotype in experimental animals

TL;DR: A partial but prolonged energy impairment induced by 3NP is sufficient to replicate most of the clinical and pathophysiological hallmarks of HD, including spontaneous choreiform and dystonic movements, frontal-type cognitive deficits, and progressive heterogeneous striatal degeneration at least partially by apoptosis.
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Chronic Morphine Induces Downregulation of Spinal Glutamate Transporters: Implications in Morphine Tolerance and Abnormal Pain Sensitivity

TL;DR: Results indicate that spinal GTs may contribute to the neural mechanisms of morphine tolerance and associated abnormal pain sensitivity by means of regulating regional glutamate homeostasis.
References
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Journal ArticleDOI

In vivo presynaptic control of dopamine release in the cat caudate nucleus--II. Facilitatory or inhibitory influence of L-glutamate.

TL;DR: Since a sustained reduction in the spontaneous release of [3H]dopamine was seen in the presence of PK 26124, the corticostriatal glutamatergic neurons appeared to exert a tonic facilitatory presynaptic influence on dopamine release.
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2-Amino-6-trifluoromethoxy benzothiazole, a possible antagonist of excitatory amino acid neurotransmission—II: Biochemical properties

TL;DR: Data suggest that PK 26124 possesses antagonistic properties of excitatory dicarboxylic amino acids, which may contribute to its anticonvulsant action.
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Excitatory amino acid-induced release of 3H-GABA from cultured mouse cerebral cortex interneurons.

TL;DR: The development of binding sites for the different EAA-receptor subtypes showed a good correlation with the development of neuronal 3H-GABA release evoked by the excitatory amino acids.
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Riluzole, a novel antiglutamate, prevents memory loss and hippocampal neuronal damage in ischemic gerbils.

TL;DR: The neuroprotective effects of riluzole, a novel antiglutamate, has been demonstrated in a model of ischemia induced in female Mongolian gerbils by transient bilateral carotid occlusion and a clear-cut correlation was found between the deficit in the memory test and the decrease in muscarinic receptor binding in the CA1 fields.
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