l homocysteine/seizures

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Synergistic inhibition of [3H]muscimol binding to calf-brain synaptic membranes in the presence of L-homocysteine and pyridoxal 5'-phosphate. A possible mechanism for homocysteine-induced seizures.

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L-Homocysteine and pyridoxal 5'-phosphate (PxyP) inhibited [3H]muscimol binding to freeze-thawed, Triton-treated calf brain membranes (containing high-affinity muscimol-binding sites: Kd 9.5 +/- 0.6 nM, Bmax 5.2 +/- 0.2 pmol/mg protein). The homocysteine--pyridoxal-5'-phosphate (Hcy-PxyP) thiazine

The effect of N-methyl-D-aspartate receptor antagonists on D,L-homocysteine thiolactone induced seizures in adult rats.

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The aim of our study was to investigate the effects of ifenprodil and MK-801 on D,L-homocysteine thiolactone induced seizures in adult rats.Male Wistar rats were divided into following groups: 1. Saline-treated (C, n=10); 2. D,L-homocysteine thiolactone 8 mmol/kg, i.p. (H, n=7); 3. Ifenprodil 20

High dose of ethanol decreases total spectral power density in seizures induced by D,L-homocysteine thiolactone in adult rats.

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The effects of ethanol on epilepsy are very complex. Ethanol can have depressant as well as excitatory effect on different animal models of epilepsy. Systemic administration of homocysteine can trigger seizures. The aim of the present study was to examine the changes of total spectral power density

The effect of diazepam on brain levels of S-adenosyl-L-methionine and S-adenosyl-L-homocysteine: possible correlation with protection from methionine sulfoximine seizures.

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Administration of the long latency convulsant, L-methionine-d,1-sulfoximine (MSO) results in an increase in brain methylation flux. We determined the effects of the anticonvulsant, diazepam (DZ) on MSO seizures and on brain levels of S-adenosyl-L-methionine (AdoMet) and S-adenosyl-L-homocysteine

The role of nitric oxide in homocysteine thiolactone-induced seizures in adult rats.

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The role of NO in epileptogenesis has been studied in different experimental models, and the reported results have been highly contradictory. The current study aimed to determine the role of NO in mechanisms of D: ,L: -homocysteine-thiolactone (H) induced seizures by testing the action of L:

Experimental secondarily generalized convulsive status epilepticus induced by D,L-homocysteine thiolactone.

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Secondarily generalized convulsive status epilepticus was induced by intraperitoneal (i.p.) injection of D,L-homocysteine thiolactone to rats with actively epileptogenic cobalt lesions in motor cortex. This induced focal motor seizures which secondarily generalized. Control animals not treated with

Inhibition of the neuronal nitric oxide synthase potentiates homocysteine thiolactone-induced seizures in adult rats.

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Nitric oxide (NO), one of the gaseous neurotransmitters, is produced in reaction catalyzed by family of NO synthases (NOS). The involvement of neuronal NOS (nNOS) in seizures induced by homocysteine thiolactone has not been studied. Therefore, the aim of this study was to determine the effects of

Two types of seizures in homocysteine thiolactone-treated adult rats, behavioral and electroencephalographic study.

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D,L-homocysteine thiolactone (H), a reactive homocysteine metabolite, contributes to total homocysteine pool. The aim of the present study was to determine the effects of H after acute application in increasing doses to rats. Adult Wistar rat were intraperitoneally administered saline or H in

Effect of L-homocysteine and derivatives on the high-affinity uptake of taurine and GABA into synaptosomes and cultured neurons and astrocytes.

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The effect of L-homocysteine and selected derivatives on the high-affinity uptake of the inhibitory neuroeffectors, GABA and taurine, was investigated in synaptosomes, and in cultured neurons and astrocytes. High-affinity uptake of taurine into synaptosomes was inhibited most effectively by

E1 mice epilepsy shows genetic polymorphism for S-Adenosyl-L-homocysteine hydrolase.

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E1 mice are an animal model of human epilepsy (idiopathic complex partial seizures). We have previously demonstrated abrupt poly(A)(+) RNA expression in liver from 1-day-old E1 mouse [Mita et al., 1991. Devl. Brain Res. 64, 27-35]. In the present study, we constructed a cDNA library of the

Differential changes in the content of amino acid neurotransmitters in discrete regions of the rat brain prior to the onset and during the course of homocysteine-induced seizures.

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Changes in amino acid concentrations were investigated in selected regions of rat brain prior to the onset and during the course of epileptiform seizures induced by L-homocysteine. The concentration of gamma-aminobutyric acid (GABA) decreased preictally in substantia nigra (-18%), caudate putamen

[S-adenosyl-L-homocysteine: 2. An anticonvulsant].

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S-Adenosyl-L-homocysteine (SAH) decreases the epileptiform discharges induced by hippocampic stimulation. SAH reduces the pentetrazol convulsions, does not modify picrotoxine convulsions, and increases strychnine toxicity. These effects are not linked to gamma-aminobutyric acid metabolism

A double inhibition kinetic analysis of [3H]-muscimol binding to the gamma-aminobutyric acid receptor on calf brain synaptic membranes. Further studies on the mechanism of homocysteine-induced seizures.

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The simultaneous action of pyridoxal 5'-phosphate (PLP) and L-homocysteine on specific [3H]muscimol binding to the gamma-aminobutyric acid receptor on freeze-thawed, Triton-treated calf-brain synaptic membranes was examined kinetically by double inhibition analysis. PLP was found to be a pure

Possible role of increased brain methylation in methionine sulfoximine epileptogenesis: effects of administration of adenosine and homocysteine thiolactone.

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An intraventricular pulse of [14COOH]L-methionine to mice pretreated with the convulsant L-methionine-dl-sulfoximine (MSO) resulted in significantly higher than control specific radioactivity values of cerebral [14COOH]L-methionine (Met), [14COOH]S-adenosyl-L-methionine (AdoMet) and

Brain methylation and epileptogenesis: the case of methionine sulfoximine.

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A brief review of the neurochemical effects of the convulsant agent L-methionine-dl-sulfoximine (MSO) on cerebral methylation reactions is presented. Our findings point to the involvement of a number of endogenous methyl acceptor molecules, including histamine, membrane phospholipids, and membrane

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