Neuronal Cell Death

penheim, 1991; Burek and Oppenheim, 1998). Although Neurons may die at many different developmental stages some of these hypotheses have received experimental and for many different reasons. As in other tissues, difsupport in individual systems, none seems to be generferent stimuli produce quite different morphological ally applicable. Indeed, it remains to be demonstrated that manifestations of cell death. Many authors have sought a single explanation exists. In the nematode C. elegans, to distinguish apoptosis (involving nuclear and cyto105 neurons (of a total of 1090 cells initially produced) plasmic condensation and intranucleosomal DNA cleavundergo cell death, allowing in some cases for generaage, followed by phagocytosis) from necrosis (involving tion of different resulting structures from similar initial swelling of mitochondria and endoplasmic reticulum lineages (Ellis and Horvitz, 1986). One role for neuronal and subsequent loss of membrane integrity). However, death that seems to be common to invertebrates and these paradigms were developed for cancer cells (Wyllie vertebrates is the creation of sexually dimorphic strucet al., 1980), and may be only partially valid for analyzing tures (Bottjer and Arnold, 1997). Elsewhere in vertecell death in the nervous system, as in some cases brates, the most generally accepted idea is that neurons aspects of both may be manifest (reviewed by Clarke, are produced “in excess” in order that they may com1998). Here, we will therefore use these terms only in pete for contacts with their cellular partners and thus theirmost general sense, todistinguish where necessary adjust their numbers so as to provide sufficient innervabetween processes that involve activation of dedicated tion of their targets. cellular suicide machinery (programmed cell death, apo-