adenosine triphosphate/seizures

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Brain adenosine triphosphate: decreased concentration precedes convulsions.

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The concentration of adenosine triphosphate in the brain decreased before the onset of generalized convulsions in unanesthetized rats subjected to acute hypoxia or treated with hydroxylamine or pentylenetetrazole (Metrazol). As the convulsive episode continued, adenosine triphosphate decreased

Prolonged neonatal seizures exacerbate hypoxic-ischemic brain damage: correlation with cerebral energy metabolism and excitatory amino acid release.

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BACKGROUND Perinatal hypoxia-ischemia (HI) is the most common precipitant of seizures in the first 24-48 h of a newborn's life. In a previous study, our laboratory developed a model of prolonged, continuous electrographic seizures in 10-day-old rat pups using kainic acid (KA) as a proconvulsant.

In vivo 31P and in vitro 1H nuclear magnetic resonance study of hypoglycemia during neonatal seizure.

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To examine the hypothesis that hypoglycemia has an adverse effect on brain energy state during seizure, neonatal dogs were subjected to bicuculline-induced seizure while hyperglycemic, normoglycemic, or hypoglycemic. Cerebral blood flow increased and remained elevated in all animals subjected to

Energy metabolism in audiogenically seizure-prone chicks.

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Female chicks carrying the lethal, sex-linked recessive paroxysmal (px) gene are susceptible to spontaneous and audiogenic seizures. Because seizure activity does not begin until 1 to 2 weeks posthatching - coincidental with disappearance of the yolk-sac - it is postulated that a contributing factor

A mitochondrial ATPase 6 mutation is associated with Leigh syndrome in a family and affects proton flow and adenosine triphosphate output when modeled in Escherichia coli.

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A multidisciplinary strategy was used to identify the molecular defect in a family with Leigh syndrome (LS). The propositus presented severe developmental delay, an ataxic-spastic gait and seizures. She died at 3.5 y of age from cardiorespiratory arrest. Postmortem examination disclosed pathological

A unifying concept of seizure onset and termination.

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Recent discoveries in molecular biology and human genetics have contributed greatly to an understanding of the nature of seizure (ictal) activity. However, two questions of fundamental clinical importance continue to resist scientific inquiry: when and why does a seizure begin; and when and why does

Event-Associated Oxygen Consumption Rate Increases ca. Five-Fold When Interictal Activity Transforms into Seizure-Like Events In Vitro.

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Neuronal injury due to seizures may result from a mismatch of energy demand and adenosine triphosphate (ATP) synthesis. However, ATP demand and oxygen consumption rates have not been accurately determined, yet, for different patterns of epileptic activity, such as interictal and ictal events. We

Cerebrospinal fluid purine metabolite and neuron-specific enolase concentrations after febrile seizures.

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If febrile seizures cause significant compromise of neuronal metabolism (whether permanent or reversible), this should be reflected in an increase in the cerebrospinal fluid concentrations of neuron-specific enolase (NSE) and/or adenosine triphosphate (ATP) breakdown products. In the present study,

Acute creatine administration improves mitochondrial membrane potential and protects against pentylenetetrazol-induced seizures.

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A growing body of evidence indicates that creatine (Cr) exerts beneficial effects on a variety of pathologies where energy metabolism and oxidative stress play an etiological role. However, the benefits of Cr treatment for epileptics are still shrouded in controversy. In the present study, we found

Relationship of serum ATPase activity and the levels of neuron- specific enolase, S100B and B-cell lymphoma/leukemia-2 with cognitive function after epileptic seizure

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Background: To analyze the relationship of serum ATPase activity and the levels of neuron-specific enolase (NSE), S100B protein and B-cell lymphoma/leukemia (Bcl)-2 with cognitive function in patients after epileptic seizure.

Purine metabolites and pyrimidine bases in cerebrospinal fluid of children with simple febrile seizures.

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Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid and pyrimidine bases were determined in the CSF of 18 children after simple febrile seizures and in a control group. There was no statistically significant difference

Cerebrospinal fluid purine metabolites after complex febrile convulsions.

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Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine and uric acid were determined in cerebrospinal fluid (CSF) of 15 children after complex febrile seizures (CFS) and in 27 after simple febrile seizures (SFS), and compared with

A hypothesis for cyanide-induced tonic seizures with supporting evidence.

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A possible relationship among cyanide-induced convulsions, calmodulin, nitric oxide and protein kinase C was investigated in mice. The ED50 value of cyanide as measured by induction of tonic seizures was significantly increased in a dose-dependent manner when mercuric chloride (0.5 or 5.0

Physiologic and metabolic alterations associated with seizures in normoxic and asphyxiated neonatal dogs.

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The effect of asphyxia on seizures was determined in neonatal dogs. In normoxic (paralyzed and ventilated) neonatal dogs, bicuculline-induced seizures produced significant elevations of arterial blood pressure, PO2, glucose, lactate, and epinephrine. Cerebral blood flow increased severalfold; brain

Intrastriatal methylmalonic acid administration induces convulsions and TBARS production, and alters Na+,K+-ATPase activity in the rat striatum and cerebral cortex.

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OBJECTIVE Methylmalonic acid (MMA) inhibits succinate dehydrogenase (SDH) and beta-hydroxybutyrate dehydrogenase activity in vitro. Acute intrastriatal administration of MMA induces convulsions through glutamatergic mechanisms probably involving primary adenosine triphosphate (ATP) depletion and

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