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putrescine/seizures

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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

Elevated seizure threshold and impaired spatial learning in transgenic mice with putrescine overproduction in the brain.

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We have studied the role of putrescine by using transgenic mouse lines overexpressing the human ornithine decarboxylase gene in most of their tissues. The aberrant expression of the transgene is most strikingly manifested in the brain, leading to an increase of up to 20-fold in putrescine content.

Involvement of putrescine in the development of kindled seizure in rats.

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During the development of kindling by daily electrical stimulations applied to the left amygdala of rats, concentrations of the polyamines putrescine, spermidine, and spermine were measured in the left amygdala and the remainder of the cerebrum. A significant increase of putrescine concentration
In our previous study, an increase in concentration of putrescine was observed in the brain of amygdaloid kindled rats. To clarify the role of putrescine in kindling, the effects of intra-amygdaloid injections of alpha-difluoromethylornithine (DFMO), an inhibitor of polyamine synthesis, or
The facilitating or antagonizing effects of polyamine analogues on N-methyl-DL-aspartate (NMDLA)-induced seizures were investigated using mice. Intracerebroventricular injection of spermidine and spermine, but not putrescine, shortened the latency to appearance of clonic convulsion induced by

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

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

Inhibition of DFMO-induced audiogenic seizures by chlordiazepoxide.

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Mice given 1% alpha-difluoromethylornithine (DFMO) in the drinking water for 5 weeks developed a hyperactive behavior characterized by uncontrolled running upon stimulation with noise. The running was followed by seizures and sometimes death. These behaviors are characteristic of audiogenic
Activation of polyamine catabolism in transgenic mice through an overexpression of spermidine/spermine N(1)-acetyltransferase (SSAT) results in a massive overaccumulation of the diamine putrescine in most tissues including brain. Putrescine pool in transgenic animals was strikingly expanded in every

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
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

One-way cross-sensitization and cross-tolerance to seizure activity from cocaine to lidocaine.

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The present study examined the effects of daily treatment with a subconvulsant dose (50 mg/kg) of cocaine or lidocaine on susceptibility to seizures induced by cross-injections of the same dose of the other local anesthetic, and to seizures induced by pentylenetetrazol (PTZ) or N-methyl-DL-aspartate

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
The motor responses (such as stereotypic behavior or convulsions induced in rats by N-methyl-D-aspartate (NMDA) administered systemically were followed by a rapid, moderate increase in the putrescine concentration in plasma which preceded an increase in this amine in the brain. This effect was not
Brain maturation and GABA metabolism are known to play a key role in epileptogenesis. The metabolism of the polyamines (putrescine, spermidine and spermine) is closely linked to the process of brain maturation. Putrescine has been shown to be catabolized to GABA in brain tissue and astrocytes. In
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