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oxidase/crise épileptique
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Anticonvulsant effects of intracerebroventricularly administered norepinephrine are potentiated in the presence of monoamine oxidase inhibition in severe seizure genetically epilepsy-prone rats (GEPR-9s).
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Pharmacological and neurochemical evidence indicates that brain noradrenergic systems play an important role in the determination of audiogenic seizure severity in genetically epilepsy-prone rats (GEPRs). In earlier studies, intracerebroventricular (ICV) injections of norepinephrine suppressed
Anti-convulsant activity of diazepam and clonidine on metaldehyde-induced seizures in mice: effects on brain gamma-amino butyric acid concentrations and monoamine oxidase activity.
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Metaldehyde when administered orally to mice at a dose of 1 g kg-1 produced convulsions and death within 2 h. Brain concentrations of gamma-aminobutyric acid (GABA) were significantly reduced and monoamine oxidase (MAO) activity significantly increased in these animals relative to controls.
Functional deficiencies of sulfite oxidase: Differential diagnoses in neonates presenting with intractable seizures and cystic encephalomalacia.
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Sulfite oxidase is a mitochondrial enzyme encoded by the SUOX gene and essential for the detoxification of sulfite which results mainly from the catabolism of sulfur-containing amino acids. Decreased activity of this enzyme can either be due to mutations in the SUOX gene or secondary to defects in
Bicuculline-induced seizures: a challenge for optical and biochemical modeling of the cytochrome oxidase CuA NIRS signal.
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The effect of seizures on brain blood flow and metabolism has been extensively studied. However, few studies have focused on mitochondria. We used near infrared spectroscopy (NIRS) to study hemoglobin and cytochrome oxidase changes during seizures, induced by the GABA antagonist bicuculline, in the
Disruption, but not overexpression of urate oxidase alters susceptibility to pentylenetetrazole- and pilocarpine-induced seizures in mice.
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There is a continuous drive to find new, improved therapies that have a different mechanism of action in order to help diminish the sizable percentage of persons with pharmacoresistant epilepsy. Uric acid is increasingly recognized as contributing to the pathophysiology of multiple disorders, and
Increase of brain endogenous monoamine oxidase inhibitory activity (tribulin) in experimental audiogenic seizures in rats: evidence for a monoamine oxidase A inhibiting component of tribulin.
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Brain tribulin activity in rats with an inherited predisposition to audiogenic epilepsy was studied after seizures of different intensity were induced by an electric bell. Weak seizures (from 0 to 2 arbitrary units) did not produce any changes in endogenous inhibitory activity towards either
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
Brain cytochrome oxidase activity after kindled seizures: a quantitative histochemical mapping study.
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Quantitative histochemistry was used to analyze changes in cytochrome oxidase (CO) activity in 93 brain regions after entorhinal cortex kindling. Rats were kindled to at least six stage-5 seizures and sacrificed either 24 h or 28 days after the last convulsion. Regional brain CO activity was
Platelet and brain GABA-transaminase and monoamine oxidase activities in patients with complex partial seizures.
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The activities of gamma-aminobutyrate aminotransferase (GABA-T) and monoamine oxidase (MAO-A and -B) were measured in blood platelets from 27 patients and hippocampal tissues from eight (GABA-T) and ten (MAO) patients with complex partial seizures. The activity of platelet GABA-T was found to be
Cytochrome c oxidase deficit is associated with the seizure onset zone in young patients with focal cortical dysplasia Type II.
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It has been postulated that mitochondrial dysfunction may be an important factor in epileptogenesis of intractable epilepsy. The current study tests the hypothesis that mitochondrial Complex IV (CIV) or cytochrome c oxidase dysfunction is associated with the seizure onset zone (SOZ) in patients with
Vigabatrin inhibits pyridoxine-5'-phosphate oxidase, not pyridoxal kinase in the hippocampus of seizure prone gerbils.
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To identify the effects of vigabatrin (VGB) on the metabolism of pyridoxal 5'-phosphate (PLP) in the seizure prone gerbil hippocampus, we conducted a chronological and comparative analysis of pyridoxal kinase (PLK) and pyridoxine-5'-phosphate oxidase (PNP oxidase) expression. In the VGB treated
Chronological changes in pyridoxine-5'-phosphate oxidase immunoreactivity in the seizure-sensitive gerbil hippocampus.
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To identify the roles of pyridoxine-5'-phosphate (PNP) oxidase in epileptogenesis and the recovery mechanisms in spontaneous seizure, a chronological and comparative analysis of PNP oxidase expression was conducted. PNP oxidase immunoreactivity in a preseizure group of seizure-sensitive (SS) gerbils
Inhibition of NADPH Oxidase Activation by Apocynin Rescues Seizure-Induced Reduction of Adult Hippocampal Neurogenesis.
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Apocynin, also known as acetovanillone, is a natural organic compound structurally related to vanillin. Apocynin is known to be an inhibitor of NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase activity and is highly effective in suppressing the production of superoxide. The
Pyridox (am) ine 5'-phosphate oxidase deficiency induces seizures in Drosophila melanogaster.
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Pyridox (am) ine 5'-phosphate oxidase (PNPO) is a rate-limiting enzyme in converting dietary vitamin B6 (VB6) to pyridoxal 5'-phosphate (PLP), the biologically active form of VB6 and involved in the synthesis of neurotransmitters including γ-aminobutyric acid (GABA), dopamine, and serotonin. In
Seizures and paroxysmal events: symptoms pointing to the diagnosis of pyridoxine-dependent epilepsy and pyridoxine phosphate oxidase deficiency.
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OBJECTIVE
We report on seizures, paroxysmal events, and electroencephalogram (EEG) findings in four female infants with pyridoxine-dependent epilepsy (PDE) and in one female with pyridoxine phosphate oxidase deficiency (PNPO).
METHODS
Videos and EEGs were analysed and compared with videos of
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