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ethanolamine/epileptisk anfald
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Incorporation of glycerol and ethanolamine into glycerophospholipid in rat brain areas during bicuculline-induced convulsive seizures.
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The effect of bicuculline-induced convulsive seizures on lipid metabolism has been studied in four brain areas (cerebellum, cerebral cortex, hippocampus, and brainstem) using [2-3H]glycerol and [1,2-14C]ethanolamine as radioactive lipid precursors administered simultaneously with bicuculline. Twelve
Anticonvulsant action of ethanolamine-O-sulphate and di-n-propylacetate and the metabolism of gamma-aminobutyric acid (GABA) in mice with audiogenic seizures.
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High levels of glycine and serine as a cause of the seizure symptoms of cavernous angiomas?
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Cavernous angiomas are vascular malformations that cause neurodegeneration and symptoms including epileptiform seizures, headache, and motor deficits. Following neurosurgical removal of the angiomas, patients mostly recover well and become seizure-free. This study reports on the levels of certain
Influence of pharmacological manipulation of inhibitory and excitatory neurotransmitter systems on seizure behavior in the Mongolian gerbil.
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The purpose of this paper was to study the relationship between different neurotransmitter systems and seizure susceptibility in Mongolian gerbils with genetically determined epilepsy. In these animals, generalized tonic-clonic seizures were induced by stimulation with a blast of compressed air. A
Monoamine and GABA metabolism and the anticonvulsant action of di-n-propylacetate and ethanolamine-O-sulphate.
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The time course of changes in behaviour, seizure response and cerebral monoamine and gamma-aminobutyric acid (GABA) metabolism has been studied in relation to the anticonvulsant actions of di-n-propylacetic acid (DPA) and ethanolamine-O-sulphate (EOS) on sound-induced seizures in DBA/2 mice. Changes
Correlation between alterations in brain GABA metabolism and seizure excitability following administration of GABA aminotransferase inhibitors and valproic acid-a re-evaluation.
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The time course of the effects of aminooxyacetic acid, ?-vinyl GABA, ?-acetylenic GABA, gabaculine, ethanolamine-O-sulphate (EOS) and valproic acid (VPA) on brain GABA content and the activities of glutamic acid decarboxylase (GAD) and GABA aminotransferase (GABA-T), the enzymes involved in
Cerebellar metabolism of phosphatidylethanolamine and its water-soluble precursors during bicuculline-induced convulsive seizures.
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The incorporation of labeled ethanolamine into phosphatidylethanolamine (PE) and its water-soluble precursors, phosphoethanolamine and CDP-ethanolamine, is measured in rat cerebella during the course of bicuculline-induced convulsive seizures. The labeling of CDP-ethanolamine and phosphoethanolamine
Chronic administration of the GABA-transaminase inhibitor ethanolamine O-sulphate leads to up-regulation of GABA binding sites.
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In rats receiving the gamma-aminobutyric acid (GABA)-transaminase inhibitor ethanolamine O-sulphate (EOS) in their drinking water for up to 28 days, the number of GABAA and GABAB binding sites was increased compared to controls. There was no change in binding affinity at GABAA or GABAB sites. One
Effect of serine and ethanolamine administration on phospholipid-related compounds and neurotransmitter amino acids in the rabbit hippocampus.
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The report concerns mechanisms for the increase of extracellular levels of ethanolamine and phosphoethanolamine in CNS regions, such as the hippocampus, in transient brain ischemia, hypoglycemia, seizures, etc. L-Serine (2.5-10 mM), D-serine (10 mM), or ethanolamine (10 mM) was administered for 20
Picrotoxin convulsions and GABA metabolism after injection of anticonvulsants in chicks.
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Two clinically effective anticonvulsants, phenobarbitone and diazepam, protected 5-day old chicks against picrotoxin convulsions without reducing brain GABA-transaminase activity or raising brain GABA concentration. Ethanolamine-O-sulphate and amino-oxyacetic acid, in doses which inhibited
Relationship between drug-induced changes in seizure thresholds and the GABA content of brain and brain nerve endings.
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The intraperitoneal administration of gabaculine, aminooxyacetic acid (s.c.), gamma-acetylenic GABA, gamma-vinyl GABA, ethanolamine-O-sulphate, sodium valproate and GABA caused significant increases in the GABA content of both the whole brain and brain nerve endings (synaptosomes) in mice, a linear
Differential sensitivity of ethanol withdrawal signs in the rat to gamma-aminobutyric acid (GABA)mimetics: blockade of audiogenic seizures but not forelimb tremors.
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Intraperitoneal injection of ethanol (1-2 g/kg) and chlordiazepoxide (2-16 mg/kg) suppressed susceptibility to audiogenically induced, clonic-tonic seizures and antagonized forelimb tremor in rats undergoing ethanol withdrawal, 30 min after treatment. However, a smaller dose of ethanol (0.5 g/kg)
The Drosophila easily shocked gene: a mutation in a phospholipid synthetic pathway causes seizure, neuronal failure, and paralysis.
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We have characterized easily shocked (eas), a Drosophila "band-sensitive" paralytic mutant. Electrophysiological recordings from flight muscles in the giant fiber pathway of adult eas flies reveal that induction of paralysis with electrical stimulation results in a brief seizure, followed by a
Rescue of easily shocked mutant seizure sensitivity in Drosophila adults.
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Genetic factors that influence seizure susceptibility can act transiently during the development of neural circuits or might be necessary for the proper functioning of existing circuits. We provide evidence that the Drosophila seizure-sensitive mutant easily shocked (eas) represents a neurological
Pathogenic Variants in PIGG Cause Intellectual Disability with Seizures and Hypotonia.
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Glycosylphosphatidylinositol (GPI) is a glycolipid that anchors >150 various proteins to the cell surface. At least 27 genes are involved in biosynthesis and transport of GPI-anchored proteins (GPI-APs). To date, mutations in 13 of these genes are known to cause inherited GPI deficiencies (IGDs),
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