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catechol/crise épileptique
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Central action of a catechol-amide seizure-inducing agent: opposing effect on tyrosine and tryptophan hydroxylase activity in vivo.
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The audiogenic seizure-inducing drug H13/04 was found to elicit opposing effects on the in vivo accumulation of 5-HTP (5-hydroxytryptophan) and DOPA (3,4-dihydroxyphenylalanine) in the brain following inhibition of L-amino acid decarboxylase. In strains of mice that normally do not exhibit
Catechol-O-methyl transferase and monoamine oxidase activities in brains of mice susceptible and resistant to audiogenic seizures.
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The activities of catechol-O-methyl transferase (COMT), monoamine oxidase (MAO), and a methanol forming enzyme were studied in whole brain homogenates and in livers obtained from DBA/2J, C57B1/6J, and F1 hybrid mice. DBA/2J mice are extremely susceptible to audiogenic seizures, whereas C57B1/6J mice
Non involvement of gamma-aminobutyric acid in catechol-induced seizures.
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The effects of certain anticonvulsant agents, namely, valproate, diazepam and phenobarbitone were investigated on catechol-induced spontaneous and evoked convulsions, in anaesthetized rats and mice. Valproate and diazepam significantly reduced the intensity of spontaneous convulsions and the
Analysis of seizures induced by a catechol-derivative.
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Proceedings: Effects of cholinergic drugs on catechol evoked convulsions.
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Proceedings: Possible central cholinergic mechanism for the production of catechol convulsions.
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Proceedings: The effects of dorsal column section on the evoked convulsions induced by catechol administration.
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The time course of brain and blood catecholamines, catechol O-methyltransferase, and amino acids in rats convulsed by oxygen at high pressure.
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The time course of changes in blood and brain catecholamines, catechol O-methyltransferase (COMT), ammonia, and amino acids leading to convulsion by high pressure oxygen breathing (OHP) in rats has been investigated. Brain catecholamines were suppressed by OHP. They changed in phase with brain COMT
The effect of the convulsant agent, catechol, on neurotransmitter uptake and release in rat brain slices.
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1 The effect of catechol on uptake and K+-stimulated release of gamma-aminobutyric acid (GABA), D-aspartate, noradrenaline and acetylcholine has been studied in slices of cerebral cortex and thalamus. 2 Low concentrations of catechol did not influence the uptake of any of the neurotransmitters in
A pharmacological study of the spontaneous convulsive activity induced by 1,2-dihydroxybenzene (catechol) in the anaesthetized mouse.
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1. The convulsive activity induced by catechol has been examined in anaesthetized mice either by determining the CD50 for the convulsions in drug-treated and control animals, or by studying the effects of various drugs on the total whole body activity. 2. The results indicate that catecholamines
Prostaglandin J2 reduces catechol-O-methyltransferase activity and enhances dopamine toxicity in neuronal cells.
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There is clear evidence that an inflammatory reaction is mounted within the CNS following trauma, stroke, infection and seizures, thus augmenting brain damage. Furthermore, chronic inflammation of the CNS is implicated in many neurodegenerative disorders. However, the effects of products of
Effects of monoamines injected into the hippocampus on hippocampal seizure discharges in the rabbit.
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The effects of intrahippocampally administered catechol- and indoleamines on the two types of hippocampal seizure discharges elicited by electrical and chemical stimulation were examined in unanesthetized rabbits. The catecholamines norepinephrine (NE) and dopamine (DA), injected into the
Differences in activity in cerebral methyltransferases and monoamine oxidases between audiogenic seizure susceptible and resistant mice and deermice.
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The specific acitivity of cerebral histamine N-methyltransferase (HMT) was significantly lower in the audiogenic seizure-susceptible (SS) 21-day old DBA/2J mouse when compared to the non-susceptible 70-day old DBA/2J mouse but not when compared to the seizure resistant (SR) C57B1/6J mouse at 21 days
Severe early-onset preeclampsia is not associated with a change in placental catechol O-methyltransferase (COMT) expression.
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The genetic deletion of catechol O-methyltransferase (COMT) in mice produces a preeclampsia-like phenotype, with mice exhibiting hypertension, proteinuria, and histological changes, consistent with human pathological features. 2-Methoxyoestradiol, a metabolite of COMT, increases human trophoblast
Monoamine metabolites, iron induced seizures, and the anticonvulsant effect of tannins.
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Intracortical injections of iron ions have been shown to induce recurrent seizures and epileptic discharges in the EEG. (-)-Epigallocatechin (EGC) and (-)-epigallocatechin-3-O-gallate (EGCG), isolated from green tea leaves, have been reported to prevent or diminish the occurrence of epileptic
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