succinic acid/seizures

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[Protective effect of succinic acid on cerebellar Purkinje cells of neonatal rats with convulsion].

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OBJECTIVE To investigate the protective effect of succinic acid (SA) on the cerebellar Purkinje cells (PCs) of neonatal rats with convulsion. METHODS A total of 120 healthy neonatal Sprague-Dawley rats aged 7 days were randomly divided into a neonatal period group and a developmental period group.

Convulsant action of intracerebroventricularly administered l-kynurenine sulphate, quinolinic acid and other derivatives of succinic acid, and effects of amino acids: structure-activity relationships.

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Succinic acid, and the derivatives which have been tested, i.e. phthalic, l-glutamic, l-aspartic, citric and laevulinic acids, in doses of 5,2,5,20,20 and 50 micrograms, respectively, as well as l-kynurenine sulphate and quinolinic acid, injected into the brain ventricles in mice, induced clonic

Inhibitory effects of succinic acid on chemical kindling and amygdala electrical kindling in rats.

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OBJECTIVE To investigate the effects and mechanism of succinic acid on pentylenetetrazol (PTZ) chemical kindling and amygdala electrical kindling in rats. METHODS PTZ chemical kindling and amygdala electrical kindling models were established in rats. The effects of succinic acid on the behavior and

Aplasia of the retinal vessels combined with optic nerve hypoplasia, neonatal epileptic seizures, and lactic acidosis due to mitochondrial complex I deficiency.

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A newborn male with mitochondrial complex I deficiency suffered from neonatal epileptic seizures, which later developed into infantile spasms. The infant was blind due to aplasia of the retinal vessels and hypoplasia of the optic nerve. There was congenital lactic acidosis, which persisted in later

Elevated Urinary Glyphosate and Clostridia Metabolites With Altered Dopamine Metabolism in Triplets With Autistic Spectrum Disorder or Suspected Seizure Disorder: A Case Study.

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BACKGROUND Autism is a neurodevelopmental disorder for which a number of genetic, environmental, and nutritional causes have been proposed. Glyphosate is used widely as a crop desiccant and as an herbicide in fields of genetically modified foods that are glyphosate resistant. Several researchers

Synthesis and anticonvulsant properties of new N-piperazinylalkyl imides of succinic acid.

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A number of N-[(4-aryl)- or (4-methyl)-l-piperazinyl)alkyl]imides of 3-aryl or 3,3-pentamethylenesuccinic acid were synthesized and tested for anticonvulsant activity in the maximum electroshock seizure (MES) and pentylenetetrazole seizure threshold (scMet) tests. Structures of the novel compounds

Synthesis and properties of new cyclic derivatives of succinic acid with anticonvulsant activity.

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The synthesis and pharmacological screening of a series of new phenylsuccinimide derivatives are described. Seven compounds of that series elicited a marked anticonvulsant activity. Among the compounds tested, interesting structures were those metasubstituted with bromine, fluorine or

Synthesis and properties of cyclic derivatives of succinic acid with anticonvulsant activity. Part 4.

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A series of new phenylsuccinimide derivatives substituted in the aromatic ring and/or at the nitrogen atom was synthesized and tested for activity against pentetrazole- and electroshock-induced convulsions.

The X-ray crystal structure of Escherichia coli succinic semialdehyde dehydrogenase; structural insights into NADP+/enzyme interactions.

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BACKGROUND In mammals succinic semialdehyde dehydrogenase (SSADH) plays an essential role in the metabolism of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) to succinic acid (SA). Deficiency of SSADH in humans results in elevated levels of GABA and gamma-Hydroxybutyric acid (GHB),

Metabolome disruption of the rat cerebrum induced by the acute toxic effects of the synthetic cannabinoid MAM-2201.

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OBJECTIVE The aim of this study is to investigate the metabolome disruption in the rat cerebrum induced by the recently abused synthetic cannabinoid MAM-2201. METHODS MAM-2201 was intraperitoneally administered to 6-week Wistar rats at 5 or 15mg/kg (n=5), and the cerebrum metabolome alteration was

[Changes in the dehydrogenase and GABA transaminase activity in the cerebral cortex during corazol kindling].

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The experiments on (CBA X C57BL/6)F1 mice have shown that regular corazol injections in subliminal doses stimulated seizure susceptibility (pharmacological kindling). Cytophotometric assay of the activity of oxidative metabolism enzymes (glutamate dehydrogenase, malate dehydrogenase, succinate

Inherited disorders of GABA metabolism.

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Gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the mammalian central nervous system, is produced from glutamic acid in a reaction catalysed by glutamic acid decarboxylase. The sequential actions of GABA-transaminase (converting GABA to succinic semialdehyde) and succinic

D-2-Hydroxyglutaric aciduria in a patient with a severe clinical phenotype and unusual MRI findings.

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We report an infant with intermittent urinary excretion of D-2-hydroxyglutaric (D-2-OHG) acid who died at the age of 10 months from cardiogenic shock due to cardiomyopathy. High urinary concentrations of D-2-OHG and succinic acid, as well as increased levels of lactic acid were detected on three

Malonyl coenzyme A decarboxylase deficiency. Clinical and biochemical findings in a second child with a more severe enzyme defect.

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A second child with a more severe deficiency of malonyl CoA decarboxylase is described. He is mildly mentally retarded and presented with vomiting, a seizure, hypoglycaemia and mild metabolic acidosis during a urinary tract infection. The urine contained increased amounts of malonic, methylmalonic,

The GABA shunt: an attractive and potential therapeutic target in the treatment of epileptic disorders.

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Epilepsy is the most common primary neurological disorder known. Epileptiform neurons undergo paroxysmal depolarization shifts (PDS), which result in the excessive sustained neuronal firing seen in epilepsy. These shifts are due to either an impairment of GABA mediated inhibition, or an enhancement

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