Inactivation of bcl-2 Results in Progressive Degeneration of Motoneurons, Sympathetic and Sensory Neurons during Early Postnatal Development
Autor: | Michael Meyer, Theologos M. Michaelidis, Jonathan D. Cooper, Michael Sendtner, Matti S. Airaksinen, Bettina Holtmann, Hans Thoenen |
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Rok vydání: | 1996 |
Předmět: |
Programmed cell death
neurotrophic factor prevents Sympathetic Nervous System Neuroscience(all) protooncogene bcl-2 Nerve Tissue Proteins Sensory system Degeneration (medical) Ciliary neurotrophic factor transgenic mice Neuroprotection Mice Neurotrophic factors Glial cell line-derived neurotrophic factor Animals lymphoid-tissues Ciliary Neurotrophic Factor Nerve Growth Factors Neurons Afferent motor-neurons protein expression programmed cell-death Motor Neurons Neurons biology Brain-Derived Neurotrophic Factor General Neuroscience Denervation Axons Mice Inbred C57BL Facial Nerve sequence similarity Animals Newborn Proto-Oncogene Proteins c-bcl-2 nervous system Mutation Nerve Degeneration developing nervous-system biology.protein targeted disruption Neuroscience Neurotrophin |
Zdroj: | University of Helsinki |
ISSN: | 0896-6273 |
DOI: | 10.1016/s0896-6273(00)80282-2 |
Popis: | 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. |
Databáze: | OpenAIRE |
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