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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biosynthesis of the polyamines spermidine and spermine and their precursor putrescine is controlled by the activity of the two key enzymes ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC). In the adult brain, polyamine synthesis is activated by a variety of physiological and pathological stimuli, resulting most prominently in an increase in ODC activity and putrescine levels. The sharp rise in putrescine levels observed following severe cellular stress is most probably the result of an increase in ODC activity and decrease in SAMDC activity or an activation of the interconversion of spermidine into putrescine via the enzymes spermidine N-acetyltransferase and polyamine oxidase. Spermidine and spermine levels are usually less affected by stress and are reduced in severely injured areas. Changes of polyamine synthesis and metabolism are most pronounced in those pathological conditions that induce cell injury, such as severe metabolic stress, exposure to neurotoxins or seizure. Putrescine levels correlate closely with the density of cell necrosis. Because of the close relationship between the extent of post-stress changes in polyamine metabolism and density of cellular injury, it has been suggested that polyamines play a role in the manifestation of structural defects. Four different mechanisms of polyamine-dependent cell injury are plausible: (1) an overactivation of calcium fluxes and neurotransmitter release in areas with an overshoot in putrescine formation; (2) disturbances of the calcium homeostasis resulting from an impairment of the calcium buffering capacity of mitochondria in regions in which spermine levels are reduced; (3) an overactivation of the NMDA receptor complex caused by a release of polyamines into the extracellular space during ischemia or after ischemia and prolonged recirculation in the tissue surrounding severely damaged areas; (4) an overproduction of hydrogen peroxide resulting from an activation of the interconversion of spermidine into putrescine via the enzymes spermidine N-acetyltransferase and polyamine oxidase. Insofar as a sharp activation of polyamine synthesis is a common response to a variety of physiological and pathological stimuli, studying stress-induced changes in polyamine synthesis and metabolism may help to elucidate the molecular mechanisms involved in the development of cell injury induced by severe stress.
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PMID:Polyamine metabolism in different pathological states of the brain. 135 85

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 N-acetylspermine in control and kainate-treated animals. The results indicate that KA-induced seizure activity has no effect on the polyamine interconversion pathway in developing rat brain.
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PMID:Effect of kainate-induced seizure activity on the polyamine interconversion pathway in juvenile rat brain. 755 38

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 enzyme spermine/spermidine acetyltransferase is increased at 8 and 16 h after kainate injection in piriform cortex and hippocampus. These results indicate that the polyamine interconversion pathway is rapidly activated in limbic areas following kainate-induced seizure activity, and suggest that this pathway might participate in the resulting neuronal damage.
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PMID:Kainate-induced seizure activity stimulates the polyamine interconversion pathway in rat brain. 808 78

The levels of polyamines, N-acetylpolyamines, and GABA in the cerebral cortex and brainstem of rat brain after completion of pentylenetetrazol (PTZ)-induced kindling were investigated. Pretreatment with the polyamine oxidase inhibitor MDL72527 caused an accumulation of N1-acetylspermidine and N1-acetylspermine in normal rats. After a kindling seizure, the levels of N-acetylpolyamines were elevated, particularly in the cerebral cortex, indicating activation of polyamine interconversion. The levels of putrescine and GABA were lower in kindled rats pretreated with MDL72527. In addition, pretreatment with MDL72527 enhanced the seizure susceptibility to PTZ in normal rats. These results suggest that the polyamine interconversion pathway is involved in brain excitability, probably through the regulation of putrescine and GABA levels.
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PMID:Pentylenetetrazol-induced kindling stimulates the polyamine interconversion pathway in rat brain. 1032 Jul 41