Trang 1 từ 44 các kết quả
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
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
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
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
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
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
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
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
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.
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
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
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
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.
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,
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