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glyceraldehyde 3 phosphate/eпилептички напад

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Selection of reference genes for real-time quantitative reverse transcription-polymerase chain reaction in hippocampal structure in a murine model of temporal lobe epilepsy with focal seizures.

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Reference genes are often used to normalize expression of data from real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and only a validation of their stability during a given experimental paradigm leads to reliable interpretations. The present study was thus designed

Elevated prodynorphin expression associated with ethanol withdrawal convulsions.

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The hypothesis that kappa-opioid system activity may in part mediate convulsions exhibited during ethanol withdrawal was tested by exposing Withdrawal Seizure-Prone (WSP) and Withdrawal Seizure-Resistant (WSR) mice to chronic ethanol. Whole brain was harvested for RNA isolation and prodynorphin mRNA

A key glycolytic enzyme plays a dual role in GABAergic neurotransmission and in human epilepsy.

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We have previously described a new endogenous phosphorylation mechanism that maintains ionotropic gamma-aminobutyric acid receptor (GABAAR) function and have shown that the kinase involved is the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). This enzyme is closely associated

Lability of GABAA receptor function in human partial epilepsy: possible relationship to hypometabolism.

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The function of the gamma-aminobutyric acid type A receptor (GABA(A)R) is maintained by endogenous phosphorylation. We have shown that the corresponding kinase is the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), using the locally produced glycolytic ATP. In addition, using

Changes in the gene and protein expression of K(ATP) channel subunits in the hippocampus of rats subjected to picrotoxin-induced kindling.

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ATP-sensitive K+ (KATP) channels couple the intracellular metabolic state to electrical activity, which is important in the control of neuronal excitability and seizure propagation. In this study, we investigated the changes in the gene and protein expression of KATP channel subunits in the brain of

Dual transgenic reporter mice as a tool for monitoring expression of glial fibrillary acidic protein.

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Glial fibrillary acidic protein (GFAP) is the major intermediate filament protein of astrocytes, and its expression changes dramatically during development and following injury. To facilitate study of the regulation of GFAP expression, we have generated dual transgenic mice expressing both firefly

Evaluating reference genes to normalize gene expression in human epileptogenic brain tissues.

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Several reference genes have been used to quantify gene expression in human epilepsy surgery tissue. However, their reliability has not been validated in detail, although this is crucial in interpreting epilepsy-related changes of gene expression. We evaluated 12 potential reference genes in

New therapeutic targets to develop molecules active in drug-resistant epilepsies.

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We have shown that the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is the kinase involved in the endogenous phosphorylation of the alpha1 subunit of the gamma-aminobutyric acid (GABA)(A) receptor (GABA(A)R), maintaining GABA(A)-R function. GABA(A)R endogenous phosphorylation

Glycogen synthesis and immunocytochemical study of fructose-1,6-biphosphatase in methionine sulfoximine epileptogenic rodent brain.

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The effects of the convulsant methionine sulfoximine (MSO) on the glucose pathway have been investigated in mouse and rat brain. The key gluconeogenic enzyme fructose-1,6-biphosphatase (FBPase) (EC 3.1.3.11) was immunostained by rat anti-FBPase antibody. The rat cortex slices were very lightly

Brain proteomics supports the role of glutamate metabolism and suggests other metabolic alterations in protein l-isoaspartyl methyltransferase (PIMT)-knockout mice.

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Protein l-isoaspartyl methyltransferase (PIMT) repairs the isoaspartyl residues (isoAsp) that originate from asparagine deamidation and aspartic acid (Asp) isomerization to Asp residues. Deletion of the gene encoding PIMT in mice (Pcmt1) leads to isoAsp accumulation in all tissues measured,

Valproic acid inhibits histone deacetylase activity and suppresses excitotoxicity-induced GAPDH nuclear accumulation and apoptotic death in neurons.

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Valproic acid (VPA), used to treat bipolar mood disorder and seizures, also inhibits histone deacetylase (HDAC). Here, we found that VPA and other HDAC inhibitors, butyrate and trichostatin A, robustly protected mature cerebellar granule cell cultures from excitotoxicity induced by SYM 2081 ((2S,

Differential changes in mGlu2 and mGlu3 gene expression following pilocarpine-induced status epilepticus: a comparative real-time PCR analysis.

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Group II metabotropic glutamate (mGlu II) receptors subtype 2 and 3 (mGlu2 and mGlu3) are subtle regulators of neuronal excitability and synaptic plasticity in the hippocampus. In recent years, researchers have investigated the potential neuroprotective and anticonvulsant effects of compounds acting

Disruption of GluR2/GAPDH Complex Interaction by TAT-GluR2NT1-3-2 Peptide Protects against Neuronal Death Induced by Epilepsy.

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OBJECTIVE Excitotoxic neuronal death induced by epilepsy is associated with α-amino-3-hydroxyl-5-methylisoxazole-4-propionate acid (AMPA) receptors. The GluR2 subunit of AMPA receptors (AMPARs) may bind with glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The GluR2/GAPDH complex co-internalizes

Depletion of reduced glutathione precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus.

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The time course and critical determinants of mitochondrial dysfunction and oxidative stress following limbic status epilepticus (SE) were investigated in hippocampal sub-regions of an electrical stimulation model in rats, at time points 4-44h after status. Mitochondrial and cytosolic enzyme

Anti-GAPDH Autoantibody Is Associated with Increased Disease Activity and Intracranial Pressure in Systemic Lupus Erythematosus.

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Systemic lupus erythematosus (SLE) is an immune disease characterized by multiorgan involvement. Neuropsychiatric systemic lupus erythematosus (NPSLE) is one of the most devastating complications of SLE, which lacks efficient diagnostic biomarkers. The recent studies on the anti-GAPDH
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