title: Physiological and induced neuronal death are not affected in NSE-bax transgenic mice.
abstract: Bax, a family member of the survival protein Bcl-2, is expressed in the nervous system during development and throughout adulthood. Bax deficiency has been demonstrated to prevent developmental and trophic factor deprivation-induced neuronal death. To further clarify the role of Bax in naturally occurring neuronal death and in neuronal death following apoptotic stimuli, we generated several lines of transgenic mice expressing the human Bax protein specifically in neurons, under the control of the neuron-specific enolase promoter. Transgene expression was first detected around E10.5 and E12.5, depending on the transgenic line. The total number of ganglion cells in the retina and of pyramidal cells in the hippocampus, both expressing the transgene, was similar in control and transgenic mice. In addition, in our model system, Bax overexpression did not appear to influence the in vitro survival of sensory neurons isolated from dorsal root ganglia after nerve grwoth factor (NFG) deprivation or the apoptotic death of motor neurons following axotomy.
authors.affiliation: The Walter & Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. bernard@wehi.edu.au
authors.forename: R
authors.initials: R
authors.lastname: Bernard
authors.forename: S
authors.initials: S
authors.lastname: Dieni
authors.forename: S
authors.initials: S
authors.lastname: Rees
authors.forename: O
authors.initials: O
authors.lastname: Bernard
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D019771:Axotomy; D015153:Blotting, Western; D002470:Cell Survival / Q000502:physiology; D004622:Embryo, Mammalian / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D008822:Mice, Transgenic; D009046:Motor Neurons / Q000378:metabolism / Q000502:physiology; D009414:Nerve Growth Factors / Q000172:deficiency; D009420:Nervous System / Q000033:anatomy & histology / Q000196:embryology / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000502:physiology*; D009475:Neurons, Afferent / Q000378:metabolism / Q000502:physiology; D010751:Phosphopyruvate Hydratase / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D017966:Pyramidal Cells / Q000378:metabolism / Q000502:physiology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000502:physiology; D051028:bcl-2-Associated X Protein
chemical_list: C494826:BAX protein, human; C494827:Bax protein, mouse; D009414:Nerve Growth Factors; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D010751:Phosphopyruvate Hydratase