purine/seizures

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Concentration of purine compounds in the cerebrospinal fluid of infants suffering from sepsis, convulsions and hydrocephalus.

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Catabolites of purine nucleotides were measured in the cerebrospinal fluid (CSF) of newborn infants with sepsis, seizures and hydrocephalus using isocratic reversed-phase HPLC. The inosine levels in the CSF of the infants with any of the illnesses were significantly higher when compared with the

Intracerebroventricular guanine-based purines protect against seizures induced by quinolinic acid in mice.

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Acute and chronic administration of the nucleoside guanosine have been shown to prevent quinolinic acid (QA) and alpha-dendrotoxin-induced seizures, as well as to impair memory and anxiety in rats and mice. In this study, we investigated the effect of i.c.v. administration of guanine-based purines

Purine seizure disorders.

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Developing antiepileptic agents that are specifically tailored to a patient's individual biochemistry has long been a goal of neurology. Three patients who had hyperuricosuria combined with a seizure disorder that failed to respond to traditional anticonvulsants are described. The patients had the

Quinolinic acid-induced seizures stimulate glutamate uptake into synaptic vesicles from rat brain: effects prevented by guanine-based purines.

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Glutamate uptake into synaptic vesicles is a vital step for glutamatergic neurotransmission. Quinolinic acid (QA) is an endogenous glutamate analog that may be involved in the etiology of epilepsy and is related to disturbances on glutamate release and uptake. Guanine-based purines (GBPs) guanosine

Minor contribution of ATP P2 receptors to electrically-evoked electrographic seizure activity in hippocampal slices: Evidence from purine biosensors and P2 receptor agonists and antagonists.

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While the position of adenosine as an endogenous anticonvulsant is well established, it is unclear to what extent its precursor, ATP, contributes to seizure activity via P2 receptors. In this study we have addressed this issue through the use of ATP biosensors and agonists and antagonists of ATP P2

Alterations in hippocampal extracellular amino acids and purine catabolites during limbic seizures induced by folate injections into the rabbit amygdala.

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The effects on hippocampal extra- and intracellular amino acids of focal injection of folic acid into the amygdala in the rabbit were studied with brain dialysis. Folate seizures were accompanied by pronounced elevations of extracellular alanine and phosphoethanolamine. The increase of extracellular

Changes in purine levels and adenosine receptors in kindled seizures in the rat.

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Adenosine is an inhibitory modulator of neuronal activity and its possible involvement in seizures is of interest. We have examined changes in adenosine, its metabolites and receptors in brains of hippocampus-kindled rats, a model of partial epilepsy. Purine levels were measured by in vivo

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,

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

Cerebrospinal fluid purine metabolites and pyrimidine bases after brief febrile convulsions.

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Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid, and pyrimidines bases were determined in cerebrospinal fluid (CSF) of 52 children after simple febrile seizures and in a control group of 63 children. There was no

[Adenylosuccinate lyase deficiency: an unusual cause of neonatal seizure].

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Adenylosuccinate lyase deficiency is an autosomal recessive inborn error of purine synthesis, which provokes epilepsy, psychomotor delay and/or autistic features. We report on two siblings with ADSL deficiency, who developed seizures on the first day of life. ADSL deficiency should be part of the

Adenylosuccinase deficiency with neonatal onset severe epileptic seizures and sudden death.

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We report a male infant with adenylosuccinase deficiency who developed epileptic seizures on the second day of life. Growth was normal and seizures were well controlled with anti-epileptic drugs. Despite axial hypotonia associated with peripheral hypertonicity he presented some development until

Guanosine and GMP prevent seizures induced by quinolinic acid in mice.

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In the mammalian CNS, glutamate and GABA are the principal neurotransmitters mediating excitatory and inhibitory synaptic events, respectively, and have been implicated in the neurobiology of seizures. Guanine-based purines, including the nucleoside guanosine and the nucleotide GMP, have been shown

Purines and neuronal excitability: links to the ketogenic diet.

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ATP and adenosine are purines that play dual roles in cell metabolism and neuronal signaling. Acting at the A(1) receptor (A(1)R) subtype, adenosine acts directly on neurons to inhibit excitability and is a powerful endogenous neuroprotective and anticonvulsant molecule. Previous research showed an

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