| First Author | Piñón LG | Year | 1997 |
| Journal | Development | Volume | 124 |
| Issue | 20 | Pages | 4173-8 |
| PubMed ID | 9374413 | Mgi Jnum | J:43775 |
| Mgi Id | MGI:1098920 | Doi | 10.1242/dev.124.20.4173 |
| Citation | Pinon LG, et al. (1997) Bcl-2 is required for cranial sensory neuron survival at defined stages of embryonic development. Development 124(20):4173-8 |
| abstractText | 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. |
