Bcl-2 is required for cranial sensory neuron survival at defined stages of embryonic development

L G P Pinon, G Middleton, Alun Millward Davies

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)

Abstract

To ascertain the role of endogenous Bcl-2 in maintaining the survival of developing neurons and modulating their responses to neurotrophins, we compared the in vitro and in vivo survival of cranial sensory neurons of wild-type and bcl-2 null mouse embryos, At the peak of naturally occurring neuronal death in the trigeminal ganglion at E14, trigeminal neurons from bcl-2(-/-) embryos initially survived in culture in response to NGF but were not sustained as well as neurons from wild-type embryos, At the end of the period of naturally occurring neuronal death at E18, Bcl-2-deficient trigeminal neurons survived with NGF as well as wild-type neurons, At E14 in vivo, the number of trigeminal neurons undergoing apoptosis was significantly greater in bcl-2(-/-) embryos, and there were significantly fewer neurons in the trigeminal ganglia of bcl-2(-/-) embryos at E16 and E18, Similar age-related changes in the responses of nodose ganglion neurons to BDNF were observed in cultures established from bcl-2(-/-) and wild-type embryos between E14 and E18, These results suggest that endogenous Bcl-2 is required for the sustained survival response of a subset of cranial sensory neurons to neurotrophins at particular stages of embryonic development and show that its absence leads to reduced numbers of these neurons in vivo.

Original languageEnglish
Pages (from-to)4173-4178
Number of pages6
JournalDevelopment
Volume124
Issue number20
Publication statusPublished - Oct 1997

Keywords

  • Bcl-2
  • neuron survival
  • sensory neuron
  • cranial neuron
  • cell death
  • mouse
  • CELL-DEATH
  • PROTOONCOGENE BCL-2
  • SYMPATHETIC NEURONS
  • TARGETED DISRUPTION
  • MICE
  • EXPRESSION
  • BRAIN
  • GENE
  • NEUROTROPHINS
  • APOPTOSIS

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