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betaine/epileptischer anfall

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Betaine (N,N,N-trimethylglycine) and N,N-dimethylglycine have been reported to have anticonvulsant properties in animals. The purpose of the present study was to determine whether these compounds can antagonize strychnine-induced seizures when administered intraperitoneally and to compare their

Effects of betaine on seizures in the rat.

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The ability of betaine to block homocysteine, pentylenetetrazol, and electroshock induced seizures in mice has previously been observed. In this study, betaine administered IP and intraventricularly to rats blocked pentylenetetrazol-induced seizures, but IP betaine did not block audiogenic seizures.
Focal epileptic seizures can in some patients be managed by inhibiting γ-aminobutyric acid (GABA) uptake via the GABA transporter 1 (GAT1) using tiagabine (Gabitril®). Synergistic anti-seizure effects achieved by inhibition of both GAT1 and the betaine/GABA transporter (BGT1) by tiagabine and

Deletion of the betaine-GABA transporter (BGT1; slc6a12) gene does not affect seizure thresholds of adult mice.

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Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian brain. Once released, it is removed from the extracellular space by cellular uptake catalyzed by GABA transporter proteins. Four GABA transporters (GAT1, GAT2, GAT3 and BGT1) have been identified. Inhibition of

Homocysteine-induced convulsions in the rat: protection by homoserine, serine, betaine, glycine and glucose.

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N,N-dimethylglycine, betaine, and seizures.

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A placebo-controlled trial of folic acid and betaine in identical twins with Angelman syndrome.

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Angelman syndrome (AS) is a neurodevelopmental disorder that is caused by maternal genetic deficiency of a gene that encodes E6-AP ubiquitin-protein ligase (gene symbol UBE3A) mapping to chromosome 15q11-q13. AS leads to stiff and jerky gait, excess laughter, seizures, and severe
Seizure activity can alter GABA transporter and osmoprotective gene expression, which may be involved in the pathogenesis of epilepsy. However, the response of the betaine/GABA transporter (BGT1) is unknown. The goal of the present study was to compare the expression of BGT1 mRNA to that of other

Anticonvulsant properties of betaine.

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It has been shown previously that convulsions induced by homocysteine are blocked by betaine. In the present study, betaine was found to block the induction of convulsions by electroconvulsive shock and by pentylenetetrazol at least at effectively as it blocked convulsions induced by homocysteine.

Role of the betaine/GABA transporter (BGT-1/GAT2) for the control of epilepsy.

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Inactivation of gamma-aminobutric acid (GABA) as a neurotransmitter is mediated by diffusion in the synaptic cleft followed by binding to transporter sites and translocation into the intracellular compartment. The GABA transporters of which four subtypes have been cloned (GAT1-4) are distributed at
The betaine/γ-aminobutyric acid (GABA) transporter 1 (BGT1) is one of the four GABA transporters (GATs) involved in the termination of GABAergic neurotransmission. Although suggested to be implicated in seizure management, the exact functional importance of BGT1 in the brain is still elusive. This
Betaine (N-trimethylglycine), a common osmolyte, has received attention because of the number of clinical reports associating betaine supplementation with improved cognition, neuroprotection and exercise physiology. However, tissue analyses report little accumulation of betaine in brain tissue
In a recent study, EF1502 [N-[4,4-bis(3-methyl-2-thienyl)-3-butenyl]-3-hydroxy-4-(methylamino)-4,5,6,7-tetrahydrobenzo [d]isoxazol-3-ol], which is an N-substituted analog of the GAT1-selective GABA uptake inhibitor exo-THPO (4-amino-4,5,6,7-tetrahydrobenzo[d]isoxazol-3-ol), was found to inhibit GABA

Long-term outcome in treated combined methylmalonic acidemia and homocystinemia.

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OBJECTIVE To describe the clinical and biochemical features and long-term outcome of a cohort of eight patients with methylmalonic acidemia and homocystinuria (cblC). METHODS Documentation of clinical features at birth and longitudinal follow-up of the biochemical and clinical response to treatment

Anticonvulsant activity and acute neurotoxic profile of Achyranthes aspera Linn.

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BACKGROUND Root powder of Achyranthes aspera Linn. (A. aspera) belongs to family Amaranthaceae is used in Indian traditional medicine for the management of epilepsy and its efficacy is widely acclaimed among the different rural communities. OBJECTIVE The present study was aimed to establish the
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