Physiological and induced neuronal death are not affected in NSE-bax transgenic mice

J Neurosci Res. 1998 May 1;52(3):247-59. doi: 10.1002/(SICI)1097-4547(19980501)52:3<247::AID-JNR1>3.0.CO;2-D.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Axotomy
  • Blotting, Western
  • Cell Survival / physiology
  • Embryo, Mammalian / metabolism
  • Gene Expression Regulation, Developmental
  • Hippocampus / cytology
  • Hippocampus / metabolism
  • Hippocampus / physiology
  • Humans
  • Immunohistochemistry
  • Mice
  • Mice, Transgenic
  • Motor Neurons / metabolism
  • Motor Neurons / physiology
  • Nerve Growth Factors / deficiency
  • Nervous System / anatomy & histology
  • Nervous System / embryology
  • Nervous System / metabolism
  • Neurons / metabolism
  • Neurons / physiology*
  • Neurons, Afferent / metabolism
  • Neurons, Afferent / physiology
  • Phosphopyruvate Hydratase / metabolism*
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
  • Pyramidal Cells / metabolism
  • Pyramidal Cells / physiology
  • Retinal Ganglion Cells / metabolism
  • Retinal Ganglion Cells / physiology
  • bcl-2-Associated X Protein


  • BAX protein, human
  • Bax protein, mouse
  • Nerve Growth Factors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • Phosphopyruvate Hydratase