title: Mitochondrial involvement in the point of no return in neuronal apoptosis.
abstract: Programmed cell death (PCD) contributes to development, maintenance, and pathology in various tissues, including the nervous system. Many molecular, biochemical, and genetic events occur within cells undergoing PCD. Some of these events are incompatible with long-term cell survival because they have irreversible, catastrophic consequences. The onset of such changes marks the point of no return, a decisive regulatory event termed 'the commitment-to-die.' In this review, we discuss events that underlie the commitment-to-die in nerve growth factor-deprivation-induced death of sympathetic neurons. Findings in this model system implicate the mitochondrion as an important site of regulation for the commitment-to-die in the presence or absence of caspase inhibition.
authors.affiliation: Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8103, St. Louis, MO 63110-1031, USA.
authors.forename: L K
authors.initials: LK
authors.lastname: Chang
authors.forename: G V
authors.initials: GV
authors.lastname: Putcha
authors.forename: M
authors.initials: M
authors.lastname: Deshmukh
authors.forename: E M
authors.initials: EM
authors.lastname: Johnson
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D061945:Caspase Inhibitors; D020169:Caspases / Q000172:deficiency / Q000235:genetics; D000081406:Peptidyl-Prolyl Isomerase F; D021983:Cyclophilins / Q000378:metabolism; D016572:Cyclosporine / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D009414:Nerve Growth Factors / Q000172:deficiency* / Q000502:physiology*; D009474:Neurons / Q000166:cytology*; D013564:Sympathetic Nervous System / Q000166:cytology*
chemical_list: D061945:Caspase Inhibitors; D000081406:Peptidyl-Prolyl Isomerase F; D004791:Enzyme Inhibitors; D009414:Nerve Growth Factors; D016572:Cyclosporine; D020169:Caspases; D021983:Cyclophilins