Elle Øtait plusieurs fois plus faible dans le groupe sans BMP que dans les groupes susmentionnØs (p=0,001). Nous concluons que la stØrilisation à l'oxyde d'Øthylne rØduit d'un tiers l'activitØ ostØoformatrice de la BMP de renne.
Abstract— dl‐Allylglycine, a potent inhibitor of glutamate decarboxylase in vivo when given intraperitoneally, causes a marked decrease in brain GABA concentration and at the same time a dramatic increase in l‐ornithine decarboxylase activity and a simultaneous decrease in S‐adenosyl‐l‐methionine decarboxylase activity followed by putrescine accumulation. It does not, however, alter the degree of GABA formation from putrescine. The timing of the recovery of glutamate decarboxylase activity after the injection of dl‐allylglycine is concomitant with that of the GABA concentration, indicating that it is probably glutamate decarboxylase that is solely responsible for making up the GABA deficit caused by dl‐allylglycine, and that the changes in polyamine metabolism are associated in some indirect way with the recovery process.
Mouse brain ornithine decarboxylase activity is about 70-fold higher at the time of birth compared with that of adult mice. Enzyme activity declines rapidly after birth and reaches the adult level by 3 weeks. Immunoreactive enzyme concentration parallels very closely the decrease of enzyme activity during the first postnatal week, remaining constant thereafter. The content of brain antizyme, the macromolecular inhibitor to ornithine decarboxylase, in turn is very low during the first 7 days and starts then to increase and at the age of 3 weeks it is about six times the level of that in newborn mice. This may explain the decrease in enzyme activity during brain maturation, and suggests the regulation of polyamine biosynthesis by an antizyme-mediated mechanism in adult brain.
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