PHYSIOLOGICAL AND INDUCED NEURONAL DEATH ARE NOT AFFECTED IN NSE-BAX TRANSGENIC MICE

Bax, a family member of the survival protein Bcl-2, is expressed in th e nervous system during development and throughout adulthood. Bar defi ciency has been demonstrated to prevent developmental and trophic fact or deprivation-induced neuronal death. To further clarify the role of Bar in naturally occurring neuronal death and in neuronal death follow ing apoptotic stimuli, we generated several lines of transgenic mice e xpressing the human Bar protein specifically in neurons, under the con trol of the neuron-specific enolase promoter. Transgene expression was first detected around E10.5 and E12.5, depending on the transgenic li ne. The total number of ganglion cells in the retina and of pyramidal cells in the hippocampus, both expressing the transgene, was similar i n control and transgenic mice. In addition, in our model system, Bar o verexpression did not appear to influence the in vitro survival of sen sory neurons isolated from dorsal root ganglia after nerve growth fact or (NFG) deprivation or the apoptotic death of motor neurons following axotomy, (C) 1998 Wiley-Liss, Inc.