BAX IS REQUIRED FOR NEURONAL DEATH AFTER TROPHIC FACTOR DEPRIVATION AND DURING DEVELOPMENT

Members of the BCL2-related family of proteins either promote or repre ss programmed cell death. BAX, a death-promoting member, heterodimeriz es with multiple death-repressing molecules, suggesting that it could prove critical to cell death. We tested whether Bar is required for ne uronal death by trophic factor deprivation and during development. Neo natal sympathetic neurons and facial motor neurons from Bax-deficient mice survived nerve growth factor deprivation and disconnection from t heir targets by axotomy, respectively. These salvaged neurons displaye d remarkable soma atrophy and reduced elaboration of neurites; yet the y responded to readdition of trophic factor with soma hypertrophy and enhanced neurite outgrowth. Bax-deficient superior cervical ganglia an d facial nuclei possessed increased numbers of neurons. Our observatio ns demonstrate that trophic factor deprivation-induced death of sympat hetic and motor neurons depends on Bax.