aspartic acid/seizures

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Sensitivity to N-methyl-D-aspartic acid-induced convulsions is genetically associated with resistance to ethanol withdrawal seizures.

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Mice genetically selected to be resistant (withdrawal-seizure resistant, WSR) or prone (withdrawal-seizure prone, WSP) to handling-induced convulsions during ethanol withdrawal were tested for sensitivity to convulsions induced by timed intravenous (i.v.) infusion of N-methyl-D-aspartic acid (NMDA).

N-Methyl-D-aspartic acid- and metaphit-induced audiogenic seizures in rat model of seizures.

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The effects of NMDA (N-methyl-D-aspartic acid) on metaphit (1-[1(3-isothiocyanatophenyl)-cyclohexyl]piperidine)-induced audiogenic seizures in adult male Wistar albino rats were studied with the aim of developing a suitable animal model of seizures. The animals were divided into four experimental

A possible role for aspartic acid in neonatal seizures.

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Aspartic acid concentration in CSF was markedly elevated in a newborn infant with severe, intractable seizures. The levels of all other amino acids in blood, urine, and CSF were within the normal range. Two of the six other siblings in this consanguineous family died in early infancy of a similar

Comparison of three administration modes for establishing a zebrafish seizure model induced by N-Methyl-D-aspartic acid

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Background: Epilepsy is a complex neurological disorder characterized by recurrent, unprovoked seizures resulting from the sudden abnormal discharge of brain neurons. It leads to transient brain dysfunction, manifested by abnormal

Audiogenic seizure susceptibility is induced by termination of continuous infusion of gamma-aminobutyric acid or an N-methyl-D-aspartic acid Antagonist into the inferior colliculus.

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The inferior colliculus (IC) is strongly implicated in seizure initiation in a genetic form of audiogenic seizures (AGS) and in AGS observed during ethanol withdrawal (ETX). Ethanol is known to block the actions of excitatory amino acids (EAA) and enhance the actions of gamma-aminobutyric acid

Comparative effects of felbamate and other compounds on N-methyl-D-aspartic acid-induced convulsions and lethality in mice.

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Felbamate and selected compounds were evaluated for their ability to protect against N-methyl-D-aspartic acid (NMDA)-induced convulsions and lethality in mice. Convulsions produced by intracerebroventricular administration of NMDA (0.8 micrograms per mouse) were antagonized by felbamate, phenytoin,

Metaphit-induced audiogenic seizures in mice: II. Studies on N-methyl-D-aspartic acid, GABA, and sodium channel receptors and on the disposition of metaphit in the brain.

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We previously demonstrated that metaphit (a phencyclidine analogue with an acylating isothiocyanate group) induces occurrence of audiogenic seizures in mice exposed to audio stimulation 24 h after metaphit administration. We have studied various receptor systems associated with excitatory and

Norbinaltorphimine protection against N-methyl-D-aspartic acid-induced convulsions and mortality.

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The kappa-selective opioid antagonist, norbinaltorphimine (Nor-BNI), was tested against convulsions and mortality induced by the excitatory amino acids, N-methyl-D-aspartic acid (NMDA), (R,S)-alpha-amino-3- hydroxy-5-methyl-4-isoxazole propionate (AMPA) and kainic acid and the gamma-aminobutyric

Antagonism of N-methyl-D,L-aspartic acid-induced convulsions by antiepileptic drugs and other agents.

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The effects of common antiepileptics, GABAmimetic drugs, excitatory amino acid antagonists as well as of clonidine, corynanthine, chlorpromazine and atropine were studied against clonic convulsions induced in mice by N-methyl-D,L-aspartic acid (NMDLA) after subcutaneous (340 mg/kg; ED97) and

Effects of inhaled toluene and 1,1,1-trichloroethane on seizures and death produced by N-methyl-D-aspartic acid in mice.

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Evidence exists that some abused solvents have N-methyl-D-aspartic acid (NMDA) antagonist activity, although which of their effects may be related to this mechanism is not well understood. The effects of toluene and 1,1,1-trichloroethane (TCE) on NMDA-induced seizures in mice were studied using

Aspartic acid release from cerebral cortical slices of E1 mice with high seizure susceptibility.

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Unlike their parent strain ddY mice, inbred mutant E1 mice are highly susceptible to convulsive seizures upon tossing stimulation. The uptake and release of [3H]aspartate by cerebral neocortical slices were investigated in non-stimulated E1 mice [E1(-)], in stimulated E1 mice [E1(+)] and also in ddY

The activity of opioid analgesics in seizure models utilizing N-methyl-DL-aspartic acid, kainic acid, bicuculline and pentylenetetrazole.

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Morphine, fentanyl and pethidine exhibited a biphasic dose response relationship with respect to their effects on seizure thresholds to bicuculline, pentylenetetrazole, N-methyl-DL-aspartate (NMDLA) and kainic acid in mice. The usual pattern was for low doses to be anticonvulsant and higher doses to

[Behavioral and electrographic changes during hippocampal--seizure induced by N-mechyl aspartic acid in cats].

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[Protection of rats against isoniazid-induced convulsions by the potassium and magnesium salts of DL-aspartic acid].

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[Protective effect of potassium and magnesium salts of DL-aspartic acid against convulsions caused by isoniazid and ammonium chloride in the rat].

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