Results 281 to 290 of about 44,335 (335)
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Clinical Experience With Excitatory Amino Acid Antagonist Drugs
Stroke, 1995BackgroundExcitotoxic damage due to excess release of neuronal glutamate is hypothesized to play a pivotal role in the pathogenesis of focal cerebral ischemia. Drugs that antagonize excitatory amino acid function are consistently neuroprotective in preclinical models of stroke, and many are now entering clinical trials.SummaryAntagonists of theN-methyl-
K W, Muir, K R, Lees
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Isomers of cyclazocine as excitatory amino acid antagonists
Neuropeptides, 1984Abstract As an N-methylaspartate antagonist on cat and frog spinal neurones, (−) cyclazocine was twice as potent as (+) cyclazocine. This stereoselectivity is similar to that of cyclazocine at sigma rather than at mu or kappa opiate receptors. Cyclazocine also reduced synaptic excitation in rat cortex.
D, Lodge +6 more
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Non-competitive antagonists of excitatory amino acid receptors
Trends in Neurosciences, 1987Abstract Non-competitive antagonists have become important tools for investigating the basic mechanisms of NMDA receptor function. Such compounds (e.g. MK-801, PCP) are thought to act at the level of the NMDA receptor-associated ion channel and many show a marked use-dependence in their antagonist properties.
John A. Kemp +2 more
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Agonists and antagonists for excitatory amino acid receptors
Trends in Neurosciences, 1987Abstract Behind the recent explosion of interest in the field, there lies a long period of relatively slow progress in the characterization of excitatory amino acid receptors. In this article, Jeff Watkins and Harry Olverman summarize the emergence of current ideas relating to receptor differentiation and describe some of the molecular features of ...
J.C. Watkins, H.J. Olverman
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Neuroprotective Actions of Excitatory Amino Acid Receptor Antagonists
1994Publisher Summary Postischemic neuronal degeneration is caused in part by overactivity of excitatory amino acid (EAA) neurotransmitter systems. Increases in extracellular glutamate levels result in glutamate receptor-mediated increases in postsynaptic intracellular calcium levels.
V L, Woodburn, G N, Woodruff
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Interactions of excitatory amino acid antagonists with conventional antiepileptic drugs
Metabolic Brain Disease, 1996Excitatory amino acid antagonists possess anticonvulsant properties in many experimental models of epilepsy and were shown to potentiate the protective activity of conventional antiepileptics against maximal electroshock-induced seizures in mice. Combined treatments of valproate with either D,L-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid or ...
S J, Czuczwar, W A, Turski, Z, Kleinrok
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Excitatory amino acid antagonists protect mice against MPP+ seizures
Synapse, 1992AbstractAdminstration of 1‐methyl‐4‐phenyl‐pyridinium ion (MPP+) into the lateral ventricle of mice induced clonic convulsions and lethality in a dose‐ and age‐dependent manner. MPP+ failed to induce seizures in 4‐day‐old mice, and the convulsant response to MPP+ was enhanced in aged mice.
L, Turski, D N, Stephens
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Excitatory amino acid antagonists protect cochlear auditory neurons from excitotoxicity
Journal of Comparative Neurology, 1994AbstractSince ischemic damage in the brain is linked to glutamate excitotoxicity, the effects of an acute exposure to glutamate, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole proprionic acid (AMPA) or N‐‐methyl‐D aspartate (NMDA) on the radial dendrites were compared with these occurring after a severe cochlear ischemia.
J L, Puel +4 more
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Structure-activity relations of dipeptide antagonists of excitatory amino acids
Neuroscience, 1984Structure-activity relations of dipeptides related to gamma-D-glutamylglycine have been investigated with respect to the ability of these substances to antagonize depolarizing responses of frog motoneurones in vitro to N-methyl-D-aspartate, kainate and quisqualate.
A W, Jones, D A, Smith, J C, Watkins
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Excitatory Amino Acid Antagonists as Novel Anticonvulsants
1986The convulsant effect of application of dicarboxylic amino acids to the cortex was first reported by Hayashi (1954). This observation suggests that antagonists of excitation induced by amino acid neurotransmitters might be anticonvulsant agents in some forms of epilepsy. Some rather weak and indeterminate anticonvulsant effects of glutamic acid diethyl
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