ouabain/seizures

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Rats with different thresholds to clonic convulsions induced by DMCM differ in the binding of [3H]-MK-801 and [3H]-ouabain in the membranes of brain regions.

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Considering the putative participation of N-methyl-D-aspartate (NMDA) receptors and the Na(+), K(+)-ATPase enzymes in the susceptibility to convulsions induced by the benzodiazepine inverse agonist methyl 6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), the present study sought to determine

Effects of manganese, calcium, magnesium and lithium on the ouabain-induced seizure.

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The effects of the intraventricularly administered cations (Mn2+, Ca2+, Mg2+ and Li+) against the seizure induced by ouabain (3 microgram) were investigated. Mn2+, Ca2+ and Mg2+ caused definite sedation and decreased locomotor activity. But Li+ was without significant behavioral effect at the doses

Lack of involvement of nitric oxide in the mechanisms of seizures and hippocampal damage produced by kainate and ouabain in rats.

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The gross behavioural, electrocortical and neuropathological effects of kainate (10 mg/kg i.p,) and ouabain (1 micrograms, given into one dorsal hippocampus) were studied in rats. The effects of these treatments on nitric oxide synthase (NOS) activity in homogenates of hippocampus and cortex were

Relationship Between Susceptibility to DMCM-Induced Generalized Motor Convulsions and Low-Affinity [3H]-Ouabain Binding in Membranes in Rat Brain.

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Epilepsy is one of the most prevalent neurological disorders worldwide, but its underlying mechanisms have not yet been clarified. Among the possible molecular mechanisms that underlie its occurrence are those that are responsible for the neuronal ionic gradient, including the transmembrane enzyme

Ouabain induced seizures: site of production and response to anticonvulsants.

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Ouabain, an inhibitor of Na+ -K" -ATP'ase, has been administered intraventricularly to rats to study the effect of impairment of membrane transport mechanisms on the genesis of seizures. Running and leaping seizures occur rapidly after injection of ouabain in a low volume (10 microliter) when the

Ouabain-induced seizures in rats: regional and subcellular localization of 3 H-ouabain associated with Na + -K + -ATPase in brain.

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Ouabain-induced seizures in rats: relationship to brain monoamines.

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Seizure activity evoked by implantation of ouabain and related drugs into cortical and subcortical regions of the rabbit brain.

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Ouabain-induced seizures in rats: suppressive effects of taurine and gamma-aminobutyric acid.

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Ouabain induced convulsions and 3H-norepinephrine metabolism in the rat brain.

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Actions of prostaglandins E1, E2, F1, alpha and F2alpha in ouabain-induced arrhythmia and maximal electroshock seizures.

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Ouabain-induced seizures in rats: modification by melatonin and melanocyte-stimulating hormone.

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Interactions of phenytoin with ouabain and other chemical convulsants.

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Phenytoin potentiated the convulsive actions of bicuculline and picrotoxin in mice, whereas the action of bemegride was neither potentiated nor antagonized. Seizures induced by intracerebral injection of ouabain were antagonized by phenytoin, as well as by phenobarbital, chlordiazepoxide and

The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus.

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Intrahippocampal injection of 1 nmol ouabain, a sodium/potassium (Na+,K(+)-)ATPase inhibitor, produced a necrotic lesion within 4 days, characterised by a massive invasion by foaming macrophages. A lower dose of ouabain (0.1 nmol) produced a more discrete lesion of all groups of neuronal perikarya

Effects of anticonvulsants and other agents on seizures induced by intracerebral L-glutamate.

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Convulsions induced in mice by intracerebral injection of L-glutamate were antagonized by phenytoin, phenobarbital, chlordiazepoxide and valproic acid. Trimethadione had only a small effect at the dose used, and ethosuximide was ineffective. The profile of interaction of glutamate with these

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