作者: G. Moonen , M. P. Grau-Wagemans , I. Selak
DOI: 10.1038/298753A0
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摘要: Neuroontogenesis results from a synchronized series of elementary events including cellular proliferation, migration, differentiation, recognition and death. Neuronal migration is key step in neural morphogenesis since inadequately located neurones may not establish the appropriate connections this lead to neuronal death or functional deficit synaptic circuits. Impairment has been implicated human pathology1 well documented animal pathology, such as weaver mutation mice2. The cerebellum small rodents particularly suited for study because subpial neuronogenesis occurs postnatally. subsequent inward postmitotic (mostly granule cells) studied using classical neuroanatomical methods, Golgi stain3, autoradiography after systemic injection 3H-thymidine4. Systematic ultrastructural investigation at different levels central nervous system species led Rakic propose radial glia hypothesis—that migrate along cells which serve guides during migration5. observation that inside densely packed neuropile prompted us consider possible role extracellular neutral proteolysis migration. We have focused on plasminogen activator (PA) serine proteases these enzymes are known be involved several phenomena involve cell tissue remodelling6. usual substrate PA plasminogen, converted plasmin, although other substrates exist7. report here both plasmin released by cultived 7-day-old rat paraflocculus, but 1-month-old adult paraflocculus (that is, migration), cerebellar neurones, account 95% cerebellum, can inhibited inhibitors PA–plasmin system.