cytochrome oxidase/epileptisk anfald

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Bicuculline-induced seizures: a challenge for optical and biochemical modeling of the cytochrome oxidase CuA NIRS signal.

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The effect of seizures on brain blood flow and metabolism has been extensively studied. However, few studies have focused on mitochondria. We used near infrared spectroscopy (NIRS) to study hemoglobin and cytochrome oxidase changes during seizures, induced by the GABA antagonist bicuculline, in the

Brain cytochrome oxidase activity after kindled seizures: a quantitative histochemical mapping study.

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Quantitative histochemistry was used to analyze changes in cytochrome oxidase (CO) activity in 93 brain regions after entorhinal cortex kindling. Rats were kindled to at least six stage-5 seizures and sacrificed either 24 h or 28 days after the last convulsion. Regional brain CO activity was

Dynamic changes in cerebral oxygenation in chemically induced seizures in rats: study by near-infrared spectrophotometry.

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Using near-infrared spectrophotometry, the redox state of copper in cytochrome oxidase, and the hemoglobin oxygenation state were measured in the rat brain in situ during and after chemically induced seizures. Pentylentetrazol (PTZ) administration caused the partial reduction of cytochrome oxidase

Long-term changes in regional brain cytochrome oxidase activity induced by electroconvulsive treatment in rats.

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Quantitative cytochrome oxidase (CO) histochemistry was used to examine brain regional metabolic effects of electroconvulsive shock-induced seizures (ECS). Rats receive a course of either eight ECS or control treatments and were sacrificed either 24 h or 28 days after the last session. Regional CO

Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity.

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We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of

Postnatal maturation of cytochrome oxidase and lactate dehydrogenase activity and age-dependent consequences of lithium-pilocarpine status epilepticus in the rat: a regional histoenzymology study.

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The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces some pathophysiological, temporal, and developmental features of human temporal lobe epilepsy. In this model, rates of cerebral glucose utilization measured by the [(14)C]2-deoxyglucose technique increased during the initial status

Glial differences between naïve withdrawal seizure-prone and -resistant mice.

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BACKGROUND Withdrawal seizure-prone (WSP) and withdrawal seizure-resistant (WSR) mice were bred in replicate (i.e., WSP-1 and WSP-2) to exhibit differences in handling-induced convulsion severity during ethanol withdrawal. METHODS We examined the role of the glutamatergic system in susceptibility to

Changes in cytochrome oxidase in the piriform cortex after status epilepticus in adult rats.

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OBJECTIVE The piriform cortex is involved in genesis and propagation of temporal lobe seizures. Degenerating neurons demonstrated by FluoroJade B staining are visible early after status epilepticus (SE) as well as after longer intervals. Furthermore, the piriform cortex is activated during an early

Regulation of cerebral blood flow (CBF) during hypoxia and epileptic seizures.

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In conclusion, our results suggest that neither the redox state of cytochrome oxidase nor adenosine are critical factors in the regulation of cerebral blood flow during arterial hypoxia and epileptic seizures.

Metabolic approach of absence seizures in a genetic model of absence epilepsy, the GAERS: study of the leucine-glutamate cycle.

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We suggest that a dysregulation of energy metabolism in the brain of genetic absence epilepsy rats from Strasbourg (GAERS) could create a specific cerebral environment that would favor the expression of spike-and-wave discharges (SWD) in the thalamocortical loop, largely dependent on glutamatergic

Expression of alternative oxidase in Drosophila ameliorates diverse phenotypes due to cytochrome oxidase deficiency.

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Mitochondrial dysfunction is a significant factor in human disease, ranging from systemic disorders of childhood to cardiomyopathy, ischaemia and neurodegeneration. Cytochrome oxidase, the terminal enzyme of the mitochondrial respiratory chain, is a frequent target. Lower eukaryotes possess

Hypometabolism precedes limbic atrophy and spontaneous recurrent seizures in a rat model of TLE.

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OBJECTIVE Temporal hypometabolism on fluorodeoxyglucose positron emission tomography (FDG-PET) is a common finding in patients with drug-resistant temporal lobe epilepsy (TLE). The pathophysiology underlying the hypometabolism, including whether it reflects a primary epileptogenic process, or

A case of Ohtahara syndrome with cytochrome oxidase deficiency.

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Ohtahara syndrome is a rare cause of epileptic seizures during the neonatal period. This is believed to be the first report of this syndrome with a specific metabolic defect. Defects in respiratory chain function may be more common than previously assumed in patients with this epilepsy syndrome.

Regional distributions of hippocampal Na+,K(+)-ATPase, cytochrome oxidase, and total protein in temporal lobe epilepsy.

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Na+,K(+)-ATPase (the sodium pump) is a ubiquitous enzyme that consumes ATP to maintain an adequate neuronal transmembrane electrical potential necessary for brain function and to dissipate ionic transients. Reductions in sodium pump function augment the sensitivity of neurons to glutamate,

Progressive cerebral degeneration of childhood with liver disease (Alpers Huttenlocher disease) with cytochrome oxidase deficiency presenting with epilepsia partialis continua as the first clinical manifestation.

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A previously healthy and normally developed 17-year-old young female presented with a sudden onset of focal motor seizure status that proved to be refractory to anticonvulsive treatment. Severe encephalopathy with visual impairment leading to blindness, mental deterioration, and predominantly left

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