Abstract

Overexpression of the proto-oncogene bcl-2 blocks programmed cell death in sympathetic and sensory neurons that normally die after the withdrawal of neurotrophic factors. The role of endogenous bcl-2 in the development and function of the peripheral and central nervous system is, however, not known. We have found that low levels of bcl-2 messenger RNA are widely distributed in the adult and developing rat brain. In situ hybridization localized bcl-2 messenger RNA in mitral cells of the olfactory bulb, granule and pyramidal neurons of hippocompus, pontine nuclei, cerebellar granule neurons, and in ependymal cells in adult rat brain, bcl-2 messenger RNA levels were higher in late prenatal development than in postnatal and adult brain. High levels of bcl-2 messenger RNA were expressed in the neuroepithelium and in the cortical plate in prenatal cortex. During postnatal development the distribution of the message resembled that found in adult brain. We have also tested the hypothesis that induction of bcl-2 messenger RNA expression might be part of the survival-promoting action of neurotrophic factors. Brain-derived neurotrophic factor, which supports survival of cultured cerebellar granule neurons, failed to influence the levels of bcl-2 messenger RNA in these cultures.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call