Ornithine decarboxylase and adenosylmethionine decarboxylase in mouse brain—effect of electrical stimulation

Pajunen, Antti; Hietala, Oili A.; Virransalo, Eeva-Liisa; Piha, R. S.

doi:10.1111/j.1471-4159.1978.tb07066.x

Cited by 68 publications

(28 citation statements)

References 23 publications

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“…Changes in brain polyamine synthesis induced by electrical stimulation have been studied by different groups (Arai et al, 1990;Hayashi et al, 1989;Pajunen et al, 1978;Russell et al, 1974;. In animals receiving an electroconvulsive shock (1 ms pulses for 1 s), ODC mRNA was significantly increased 2.5 h after shock and remained high for up to 24 h .…”

Section: Electrical Stimulationmentioning

confidence: 99%

“…Electrical stimulation of the mouse brain produced a sharp (approximately 7-fold) increase in ODC activity peaking at about 6 h after electroshock, and a smaller rise in SAMDC activity peaking twice at about 8 h and 24 h after electrical stimulation (Pajunen et al, 1978). Subseizure stimulation of the hippocampus (by unilateral electrical stimulation of the Schaffer-collateral axonal system; Arai et al, 1990) produced an approximately 2-fold increase in ODC activity in the hippocampus, olfactory cortex, and olfactory bulb of both hemispheres and in the cerebral cortex of the contralateral hemisphere.…”

Section: Electrical Stimulationmentioning

confidence: 99%

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Polyamine metabolism in different pathological states of the brain

Paschen

1992

Molecular and Chemical Neuropathology

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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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Section: Electrical Stimulationmentioning

confidence: 99%

Section: Electrical Stimulationmentioning

confidence: 99%

Polyamine metabolism in different pathological states of the brain

Paschen

1992

Molecular and Chemical Neuropathology

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“…Ornithine decarboxylase, a highly inducible enzyme with a very short half-life ( < 10 min), is present at very small concentrations in the adult brain (Russell and Snyder, 1969). The levels of activity of cerebral ornithine decarboxylase are induced very rapidly in response to a variety of stimuli, such as mechanical injury, intense electrical stimulation or chemical toxicity (Dienel and Cruz, 1984;Pajunen, Hietala, Virransalo and Piha, 1978). The rapid responses of omithine decarboxylase to any change in the neuronal environment, implies a relationship between these biogenic compounds and the adaptive mechanisms of the central nervous system.…”

mentioning

confidence: 99%

Differential effects of difluoromethylornithine on basal and induced activity of cerebral ornithine decarboxylase and mRNA

1991

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Summary-The induction of the activity of cerebral ornithine decarboxylase (EC 4.1.1.17) and mRNA by electrical stimulation exhibits regional differences. The effects of the enzyme inhibitor difluoromethylornithine on these regional variations was examined. Administration of this inhibitor resulted in pronounced depression of both basal and induced activity of ornithine decarboxylase in the hippocampus. Basal activity of the enzyme in the neocortex and the cerebellum appeared to be resistant to difluoromethylornithine but the induced enzyme activity was sensitive to the effects ofthis inhibitor. Susceptibility to difluoromethylornithine may be directly correlated with a slower turnover rate for ornithine decarboxylase. These results suggest that ornithine decarboxylase in the hippocampus may possess a longer half-life than its counterparts in other regions of the brain. Pretreatment with difluoromethylornithine had no effect on the induced ornithine decarboxylase mRNA in the neocortex. Thus, elevated activity of ornithine decarboxylase enzyme, due to electrical stimulation, appears to not have any effect on either the transcription or the decay rate of the induced ornithine decarboxylase mRNA. These findings support the concept of region-specific regulation of cerebral ornithine decarboxylase.

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“…Polyamines are known to affect acetyl cholinesterase activity [12], Spermidine and spermine are released from the precentral gyrus of Macacoa mulatto after electrical stim ulation [20]. A strong activation of ornithine decarboxylase (ODC; EC 4.1.1.17) as well as S-adenosylmethionine-decarboxylase (EC 4.1.1.50) has been observed in the mouse brain after electrical stimulation [17]. In mammals, the occurrence of the polyamine cadaverine ( 1,5-diaminopentane), the homolo gue of putrescine, has been entirely related to bacterial decarboxylation of lysine in the in testines [I, 33-35].…”

Section: Introductionmentioning

confidence: 99%

<i>In vitro </i>Formation of Piperidine, Cadaverine and Pipecolic Acid in Chick and Mouse Brain during Development

1978

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We have demonstrated for the first time in vitro formation of cadaverine and pipecolid acid from L-lysine in (a) chick embryos and chick embryo heads at 3–7 days of incubation (d.i.) and 5–7 d.i., respectively; (b) brain of chick embryos from 11 d.i. to 30 days after hatching (d.a.h.) for cadaverine and from 20 d.i. to 30 d.a.h. for pipecolic acid; (c) mouse brain from 2 days after birth up to 3 months after birth; and (d) mouse embryos at days 17–20 of gestation for cadaverine and at days 13 and 17 of gestation for pipecolic acid. No in vitro formation of piperidine from L-lysine could be found in either chick or mouse embryos. Only the large intestine of the chick with its contents was able to form piperidine from L-lysine at 30 d.a.h. Neither chick nor mouse embryos were able to form piperidine from cadaverine at any stage of development investigated. Piperidine was formed in very small amounts from D,L-pipecolic acid only in the brain of chick at 16 d.a.h. and in the large intestine with its contents at 30 d.a.h. The first demonstration of cadaverine and pipecolic acid biosynthesis in the avian and mammalian brain adds further support to a possible neural role of these two substances.

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Ornithine decarboxylase and adenosylmethionine decarboxylase in mouse brain—effect of electrical stimulation

Cited by 68 publications

References 23 publications

Polyamine metabolism in different pathological states of the brain

Polyamine metabolism in different pathological states of the brain

Differential effects of difluoromethylornithine on basal and induced activity of cerebral ornithine decarboxylase and mRNA

<i>In vitro </i>Formation of Piperidine, Cadaverine and Pipecolic Acid in Chick and Mouse Brain during Development

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