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polyamine/癲癇性発作

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Increases in brain polyamine concentrations in chemical kindling and single convulsion induced by pentylenetetrazol in rats.

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Concentrations of the polyamines, putrescine, spermidine and spermine were investigated in rat brains, in which chemical kindling or single convulsion had been induced by intraperitoneal injection of pentylenetetrazol (PTZ). A single injection of 60 mg/kg of PTZ produced tonic-clonic convulsion and
Systemic intraperitoneal administration of polyamine agonist IEM-1460 containing the Me3N(+) group with a stable positive charge preventing permeation of this substance through the blood-brain barrier and polyamine antagonist arcaine had no effect on the development of seizures caused by

Effect of one hyperbaric oxygen-induced convulsion on cortical polyamine content in two strains of mice.

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In rat striatum, after one hyperbaric oxygen (HBO)-induced convulsion, polyamine changes are found that could promote N-methyl-D-aspartate (NMDA) activation. In the HBO-sensitive CD1 mouse, unlike in the common C57 strain, there is some support for NMDA activation after the HBO seizure. We measured

Oral administration of glycine and polyamine receptor antagonists blocks ethanol withdrawal seizures.

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Cessation of chronic administration of orally administered large amounts of ethanol for 7 days resulted in a markedly increased frequency of audiogenic seizures in Sprague-Dawley rats. Oral administration of the novel glycine receptor antagonist, L-701,324, produced a dose-dependent (2.5 and 5.0

Seizure activity-induced changes in polyamine metabolism and neuronal pathology during the postnatal period in rat brain.

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Systemic injection of kainic acid (KA) does not cause neuronal pathology in limbic structures in rat brain prior to postnatal day (PND) 21. The present study tested if the development of the pathogenic response is associated with the maturation of a link between seizure activity and polyamine

Changes in polyamine levels and spectrin degradation following kainate-induced seizure activity: effect of difluoromethylornithine.

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The induction of ornithine decarboxylase (ODC) in adult CNS and the resulting changes in polyamine levels are often observed under conditions associated with activation of NMDA receptors, calpain stimulation and spectrin degradation. The present study was directed at evaluating the links between

Increased polyamine levels and changes in the sensitivity to convulsions during chronic treatment with cocaine in mice.

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Polyamines have been demonstrated to modulate seizure activity in animals. Repeated administration of a subthreshold dose of cocaine resulted in the development of sensitization to cocaine-induced seizures during an initial 3 or 4 days, followed by the development of tolerance to seizures on days 5

Effect of kainate-induced seizure activity on the polyamine interconversion pathway in juvenile rat brain.

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The activity of the polyamine interconversion pathway was investigated in the hippocampus and piriform cortex after systemic KA administration in juvenile rats. Pretreatment of 7-day-old rats with the polyamine oxidase inhibitor, MDL 72527, induced a similar accumulation of N-acetylspermidine and

Kainate-induced seizure activity stimulates the polyamine interconversion pathway in rat brain.

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Systemic injection of kainic acid in adult rat is accompanied by a large increase in the accumulation of acetylated derivatives of spermidine and spermine in the hippocampus and piriform cortex of animals pretreated with the polyamine oxidase inhibitor, MDL 72527. Furthermore, the activity of the

Ornithine decarboxylase induction and polyamine synthesis in the kindling of seizures: the effect of alpha-difluoromethylornithine.

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It has been suggested that the kindling of seizures may depend on the induction of genes encoding enzymes involved in neurotransmission. Experimental seizures are followed by an especially rapid and massive induction of brain ornithine decarboxylase (ODC), an enzyme which catalyses the rate-limiting

Mygalin: a new anticonvulsant polyamine in acute seizure model and neuroethological schedule.

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Polyamines are compounds that interact with ionotropic receptors, mainly modulating the NMDA receptor, which is strictly related to many neurologic diseases such as epilepsy. Consequently, polyamines rise as potential neuropharmacological tools in the prospection of new therapeutic drugs. In this

The biosynthesis of polyamines in the brain of audiogenic seizure-susceptible and -resistant deermice.

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Traxoprodil decreases pentylenetetrazol-induced seizures.

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Polyamines, including spermidine, facilitate seizures by positively modulating N-methyl-d-aspartate receptors (NMDAr). Although NMDAr antagonists decrease seizures, it remains to be determined whether traxoprodil, a selective antagonist at the NR2B subunit of the NMDAr, decreases seizures and

Polyamine metabolism and glutamate receptor agonists-mediated excitotoxicity in the rat brain.

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Putrescine (PUT) increases have been seen in a range of models of neuropathological disturbances. The present study was designed to compare the ability of various types of glutamate receptor agonist to promote excitotoxic brain damage and to examine whether a PUT increase is a general marker of

Antagonists of N-methyl-D-aspartate receptors block seizures induced by putrescine in the deep prepiriform cortex.

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The role of excitatory amino acid receptors in the genesis of motor and electrocortical seizures, elicited by administration of the polyamine putrescine into the deep prepiriform cortex, has been evaluated in rats. Motor and electrocortical seizures occurred in rats receiving unilateral local
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