TY - JOUR
T1 - Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development
AU - Michaelidis, T. M.
AU - Sendtner, M.
AU - Cooper, J. D.
AU - Airaksinen, M. S.
AU - Holtmann, B.
AU - Meyer, M.
AU - Thoenen, H.
N1 - Funding Information:
We thank Dr. R. Kemler for providing D3 embryonic stem cells and Dr. G. Evan for the Bcl-2 antiserum. We thank H. Wilde-Launert and M. Krug for excellent care of the stem cell cultures, and B. Kunkel for accomplished animal care. We also thank W. Komp, Heike Döppler, and Michaela Lederer for expert preparation of histological sections; E. Wolf, N. Brusis, and J. Richter for excellent assistance; J. Chalcroft and R. Schorner for their help with photography; Y.-A. Barde, B. Berninger, D.W. Ethell, and G. Tzimagiorgis for valuable criticism and comments on the manuscript; A.J. Barnwell for linguistic revision, and I. Hajjar for secretarial assistance. We also thank Regeneron Pharmaceuticals, Tarrytown, NY, for recombinant CNTF (Sciatin) and BDNF. T. M. M. and J. D. C. are recipients of postdoctoral fellowships from the Human Capital and Mobility program of the European Commission. M. S. was supported by the Deutsche Forschungsgemeinschaft, Grant to 61/8–1. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 USC Section 1734 solely to indicate this fact.
PY - 1996/7
Y1 - 1996/7
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=1842456916&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(00)80282-2
DO - 10.1016/S0896-6273(00)80282-2
M3 - Article
C2 - 8755480
AN - SCOPUS:1842456916
SN - 0896-6273
VL - 17
SP - 75
EP - 89
JO - Neuron
JF - Neuron
IS - 1
ER -