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Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development.

Abstract：

: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.

journal_name

Neuron

journal_title

Neuron

authors

Michaelidis TM,Sendtner M,Cooper JD,Airaksinen MS,Holtmann B,Meyer M,Thoenen H

doi

10.1016/s0896-6273(00)80282-2

subject

Has Abstract

pub_date

1996-07-01 00:00:00

pages

75-89

issue

1

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(00)80282-2

journal_volume

17

pub_type

杂志文章

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