Physiological and induced neuronal death are not affected in NSE-bax transgenic mice
- Author(s)
- Bernard, R; Dieni, S; Rees, S; Bernard, O;
- Details
- Publication Year 1998-05-01,Volume 52,Issue #3,Page 247-259
- Journal Title
- JOURNAL OF NEUROSCIENCE RESEARCH
- Publication Type
- Journal Article
- 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 growth factor (NFG) deprivation or the apoptotic death of motor neurons following axotomy, (C) 1998 Wiley-Liss, Inc.
- Publisher
- WILEY-LISS
- Keywords
- INDUCED CELL-DEATH; NEUROTROPHIC FACTOR PREVENTS; BCL-2 HOMOLOG BAK; MOTOR-NEURONS; IN-VIVO; SYMPATHETIC NEURONS; NERVOUS-SYSTEM; MOTONEURON DEATH; DEFICIENT MICE; TROPHIC FACTOR
- Publisher's Version
- https://doi.org/10.1002/(SICI)1097-4547(19980501)52:3<247::AID-JNR1>3.0.CO;2-D
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1998-05-01 12:00:00