摘要：

Cell death during the ontogeny of the nervous system allows for competitive innervation of targets (Hamburger and Oppenheim, 1982; Levi-Montalcini, 1987). Neurons that successfully compete for target-derived trophic factors, such as NGF, at critical stages in development are spared cell death. Exogenous NGF, or its withdrawal by anti-NGF, has permanent effects on survival of peripheral and striatal neurons (Levi-Montalcini, 1987; Perez-Polo, 1987). The relationship between developmental neuronal cell death and its counterparts after injury or during aging in CNS is not known. Since neurons have low endogenous levels of antioxidants, NGF effects on oxidant-antioxidant balance in the CNS can affect neuronal survival after mechanical trauma, ischemia, and reperfusion injury. Since neuronal cell death is an end point of more than one physiologic process, NGF activity may be but one of several regulatory processes at work. The NGF effect on oxidant-antioxidant balance may be but one of several mechanisms by which NGF regulates neuronal survival.

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