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inosine/seizures

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In adult male albino BALB/c mice inosine (INS, 100 and 200 micrograms, intraventricularly) prolonged the latency of pentylenetetrazol (PTZ) seizures while nicotinamide (NAM) exerted an opposite effect. In adult male C57BL/6 mice INS decreased lethality after PTZ while NAM increased it. In adult male
Nicotinamide (NAM, 1000 mg/kg), inosine (INS, 1000 mg/kg), hypoxanthine (HXT, 500 mg/kg), putative endogenous ligands of the benzodiazepine receptor, and nicotinic acid (NA, 500 mg/kg) diminished DL-kynurenine-(DL-K, 50 micrograms ICV) induced seizures in C57BL/6 adult male mice and only prolonged
Inosine (INO) has an anticonvulsant effect against seizures induced by antagonists of GABAergic system. Quinolinic acid (QA) is an agonist NMDA receptors implicated in the neurobiology of seizures. In the present study, we investigated the anticonvulsant effect of intracerebroventricular (i.c.v.)

Inosine, an endogenous ligand of the brain benzodiazepine receptor, antagonizes pentylenetetrazole-evoked seizures.

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Partially purified extracts of bovine brain were previously found to inhibit competitively the binding of [3H]-diazepam to rat brain synaptosomal membranes. The purines inosine and hypoxanthine were subsequently identified as the compounds responsible for this inhibitory activity.

Effect of inosine on seizures induced with pentylenetetrazole, bicuculline, or picrotoxin.

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The effect in mice of inosine administered subcutaneously on the threshold of seizures induced with pentylenetetrazole (PTZ), bicuculline, and picrotoxin was studied, and brain inosine levels were measured. Following inosine, 1,000 mg/kg, the threshold to PTZ was increased at 10-30 min after

The benzodiazepines and inosine antagonize caffeine-induced seizures.

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The induction of generalized tonic-clinic seizures in mice by the methylxanthine stimulant caffeine is described. These seizures are indistinguishable in quality from those induced by pentylenetetrazol (PTZ), and pretreatment with low doses of caffeine potentiates PTZ-induced seizures.

Pentylenetetrazol seizures in mice: effect on brain inosine and hypoxanthine.

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Brain inosine and hypoxanthine were measured in mice at intervals following the intraperitoneal injection of pentylenetetrazol (PTZ), 100 mg/kg. These purines increased only after myoclonic jerks appeared and were maximal at the time of tonic hindlimb extension. Phenytoin and phenobarbital, which

Inosine, hypoxanthine, and seizures.

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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
We analyzed brain tissue in 139 rats for adenosine and its metabolites, inosine and hypoxanthine, during the initial 120 seconds of seizures induced by bicuculline. We also measured ATP, ADP, AMP, phosphocreatine (PCr), and lactate. We divided the rats into four groups by adjustment of their

Adenosine deaminase in convulsions along with its regional, cellular and synaptosomal distribution in rat brain.

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Adenosine deaminase activity was determined in enriched neuronal, glial and synaptosomal fractions in three regions of rat brain. It was found to be equally distributed in cortical neurons and synaptosomes. Appreciable activity was observed in glial cells. A significant increase in the activity of

Electroshock raises pentylenetetrazol threshold: possible role of inosine.

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A series of 15 single electroshocks administered through electrodes applied to the scalp of mice raised the threshold to pentylenetetrazol-induced seizures as determined by a tail vein infusion method. The same stimulus increased brain inosine and hypoxanthine. Phenytoin, which blocks the increase

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,
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

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
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