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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.
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
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
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
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
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
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
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.
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),
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
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
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
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
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,
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