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Oxygen-induced seizures and inhibition of human glutamate decarboxylase and porcine cysteine sulfinic acid decarboxylase by oxygen and nitric oxide.
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The recombinant forms of the two human isozymes of glutamate decarboxylase, GAD65 and GAD67, are potently and reversibly inhibited by molecular oxygen (Ki = 0.46 and 0.29 mM, respectively). Inhibition of the vesicle-associated glutamate decarboxylase (GAD65) by molecular oxygen is likely to result
Melatonin attenuates L-cysteine-induced seizures and lipid peroxidation in the brain of mice.
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The effect of melatonin, a potent free radical scavenger, on L-cysteine-induced seizures and lipid peroxidation was investigated in mice. When L-cysteine (1.25, or 5.0 mumol/animal) was injected intracerebroventricularly (i.c.v.) into mice, severe tonic seizures were observed for over 20 sec in 75%
Preventive effect of N(G)-nitro-L-arginine against L-cysteine-induced seizures in mice.
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The effect of N(G)-nitro-L-arginine (NNA), an inhibitor of nitric oxide (NO) synthase on L-cysteine- induced neurotoxicity was investigated in mice. When L-cysteine (1, 2.5, 5 or 10 micromol/brain) was injected intracerebroventricular (i.c.v.) in mice, severe tonic seizures were observed for over 20
Lack of the alanine-serine-cysteine transporter 1 causes tremors, seizures, and early postnatal death in mice.
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The Na(+)-independent alanine-serine-cysteine transporter 1 (Asc-1) is exclusively expressed in neuronal structures throughout the central nervous system (CNS). Asc-1 transports small neutral amino acids with high affinity especially for D-serine and glycine (K(i): 8-12 microM), two endogenous
Selenium cysteine and epileptic seizures.
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PDI Knockdown Inhibits Seizure Activity in Acute Seizure and Chronic Epilepsy Rat Models via S-Nitrosylation-Independent Thiolation on NMDA Receptor.
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Redox modulation and S-nitrosylation of cysteine residues are the post-translational modifications of N-methyl-D-aspartate receptor (NMDAR) to regulate its functionality. Recently, we have reported that protein disulfide isomerase (PDI) reduces disulfide bond (S-S) to free thiol (-SH)
PDI regulates seizure activity via NMDA receptor redox in rats.
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Redox modulation of cysteine residues is one of the post-translational modifications of N-methyl-D-aspartate receptor (NMDAR). Protein disulfide isomerases (PDI), an endoplasmic reticulum (ER) chaperone, plays a crucial role in catalyzing disulfide bond formation, reduction, and isomerization. In
Cysteine-induced hypoglycemic brain damage: an alternative mechanism to excitotoxicity.
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Central neural damage caused by L-cysteine (L-Cys) was first reported more than 30 years ago. Nevertheless, the exact mechanisms of L-Cys-mediated neurotoxicity are still unclear. Preliminary study in mice demonstrated that, following L-Cys injection, animals developed tachypnea, tremor,
Plasma cysteine/cystine redox couple disruption in animal models of temporal lobe epilepsy.
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Currently the field of epilepsy lacks peripheral blood-based biomarkers that could predict the onset or progression of chronic seizures following an epileptogenic injury. Thiol/disulfide ratios have been shown to provide a sensitive means of assessing the systemic redox potential in tissue and
Control of seizures by ketogenic diet-induced modulation of metabolic pathways.
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Epilepsy is too complex to be considered as a disease; it is more of a syndrome, characterized by seizures, which can be caused by a diverse array of afflictions. As such, drug interventions that target a single biological pathway will only help the specific individuals where that drug's mechanism
A patient with pycnodysostosis presenting with seizures and porencephalic cysts.
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Pycnodysostosis is a rare autosomal recessive disorder caused by mutations in the cysteine protease Cathepsin K gene located on chromosome 1q21. It has a well characterized skeletal phenotype which include short stature, generalized increased bone density with propensity of fractures, open calvarial
Association between variation in the human KCNJ10 potassium ion channel gene and seizure susceptibility.
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OBJECTIVE
Our research program uses genetic linkage and association analysis to identify human seizure sensitivity and resistance alleles. Quantitative trait loci mapping in mice led to identification of genetic variation in the potassium ion channel gene Kcnj10, implicating it as a putative seizure
Neuroprotection of co-activation of GABA receptors by preventing caspase-3 denitrosylation in KA-induced seizures.
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Previous studies have demonstrated that kainic acid (KA)-induced seizures can cause the enhancement of excitation and lead to neuronal death in rat hippocampus. Co-activation of the inhibitory GABA receptors can attenuate the excitatory JNK3 apoptotic signaling pathway via inhibiting the increased
Involvement of caspase-3-like protease in the mechanism of cell death following focally evoked limbic seizures.
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The cysteine protease caspase-3 may be involved in the mechanism of cell death following seizures. Using a rat model of focally evoked limbic epilepsy with continuous electroencephalography monitoring, we investigated seizure-induced changes in caspase-3 protein expression and processing, enzyme
Transgenic mice neuronally expressing baculoviral p35 are resistant to diverse types of induced apoptosis, including seizure-associated neurodegeneration.
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Apoptosis is a cell-suicide process that appears to play a central role not only during normal neuronal development but also in several neuropathological disease states. An important component of this process is a proteolytic cascade involving a family of cysteine proteases called caspases. Caspase
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