Bcl-2 influences axonal growth rate in embryonic sensory neurons

Curr Biol. 1997 Oct 1;7(10):798-800. doi: 10.1016/s0960-9822(06)00339-3.


Bcl-2 plays a key role in regulating cell survival in the immune and nervous systems. Mice lacking the bcl-2 gene have markedly reduced numbers of B and T cells as a result of increased apoptosis, whereas mice with a transgene causing high levels of Bcl-2 expression in the immune system show extended survival of B and T cells. Overexpression of Bcl-2 in cultured neurons prevents their death following neurotrophin deprivation, and mice with a bcl-2 transgene under the control of a neuron-specific enolase promoter have increased numbers of neurons in several regions. Cultured neurons expressing antisense bcl-2 RNA have an attenuated survival response to neurotrophins, and neurons of postnatal bcl-2-deficient mice die more rapidly following NGF deprivation in vitro and are present in reduced numbers in vivo. Here, we show that Bcl-2 also plays a role in regulating axonal growth rates in embryonic neurons. Sensory neurons from the trigeminal ganglia of bcl-2-deficient mouse embryos, removed from the embryo on embryonic day 11 or 12, extend axons more slowly in vitro than do neurons from wild-type embryos of the same age. Serial measurements of axonal length in the same neurons revealed that there were marked differences in axonal growth rate between bcl-2-deficient and wild-type neurons, irrespective of whether the neurons were grown with nerve growth factor, brain-derived neurotrophic factor or neurotrophin-3. Because there was no significant difference in the numbers of wild-type and bcl-2-deficient neurons surviving with each neurotrophin at this early stage of development, the effect of Bcl-2 on axonal growth rate is not a consequence of its well documented role in preventing apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons*
  • Brain-Derived Neurotrophic Factor / pharmacology
  • Cell Division / drug effects
  • Cell Division / physiology
  • Mice
  • Nerve Growth Factors / pharmacology
  • Neurons, Afferent / cytology*
  • Neurons, Afferent / drug effects
  • Neurons, Afferent / metabolism
  • Neurotrophin 3
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • Trigeminal Ganglion / cytology
  • Trigeminal Ganglion / embryology


  • Brain-Derived Neurotrophic Factor
  • Nerve Growth Factors
  • Neurotrophin 3
  • Proto-Oncogene Proteins c-bcl-2