Michaelidis T M, Sendtner M, Cooper J D, Airaksinen M S, Holtmann B, Meyer M, Thoenen H
Department of Neurochemistry, Max-Planck-Institute for Psychiatry, Planegg-Martinsried, Federal Republic of Germany.
Neuron. 1996 Jul;17(1):75-89. doi: 10.1016/s0896-6273(00)80282-2.
Bcl-2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. To assess whether Bcl-2 is involved in regulating neuronal survival and in mediating the neuroprotective action of neurotrophic factors, we generated Bcl-2-deficient mice. At birth, the number of facial motoneurons, sensory, and sympathetic neurons was not significantly changed, and axotomy-induced degeneration of facial motoneurons could still be prevented by brain-derived neurotrophic factor (BDNF) or ciliary neurotrophic factor (CNTF). Interestingly, substantial degeneration of motoneurons, sensory, and sympathetic neurons occurred after the physiological cell death period. Accordingly, Bcl-2 is not a permissive factor for the action of neurotrophic factors, and although it does not influence prenatal neuronal survival, it is crucial for the maintenance of specific populations of neurons during the early postnatal period.
Bcl-2是程序性细胞死亡的主要调节因子，而程序性细胞死亡是塑造发育中的神经系统的关键过程。为了评估Bcl-2是否参与调节神经元存活以及介导神经营养因子的神经保护作用，我们培育了Bcl-2基因缺陷小鼠。出生时，面神经运动神经元、感觉神经元和交感神经元的数量没有显著变化，脑源性神经营养因子（BDNF）或睫状神经营养因子（CNTF）仍可预防轴突切断诱导的面神经运动神经元变性。有趣的是，在生理性细胞死亡期后，运动神经元、感觉神经元和交感神经元出现了大量变性。因此，Bcl-2不是神经营养因子作用的许可因子，虽然它不影响产前神经元存活，但对出生后早期特定神经元群体的维持至关重要。
