Nerve growth factor (NGF) is considered to be a target-derived survival or differentiation factor for neural crest cells of the sympathoadrenal lineage. However, exogenous NGF was found to have a positive effect on the size of the primary sympathetic ganglia (PSG) of the chick embryo, well before sympathetic innervation of the periphery. We have determined the cellular mechanism of NGF's action on the PSG by quantifying both proliferation and apoptosis. The proportion of PSG cells in S-phase is nearly double in NGF-treated embryos compared to that in controls, strongly suggesting that NGF acts as a mitogenic factor. NGF reduced the low level of apoptosis at this stage as well. Since trkA has not been detected in the avian sympathetic ganglia until later in development, we suggest that these early effects of exogenous NGF may be mediated by the low-affinity neurotrophin receptor, p75, which is expressed from neural crest migration stages.
Bibliographical noteFunding Information:
Our thanks to Professor Ron Oppenheim for critical reading of the manuscript. This work was supported by the Health Science Center at Bar-Ilan University, the Aviv Fund for Neuroscience Research, and the Dysautonomia Foundation Inc. The anti-BrDU antibodies were obtained from the Developmental Studies Hybridoma Bank maintained by the Department of Pharmacology and Molecular Sciences, Johns Hopkins University, and the Department of Biological Sciences, University of Iowa, under Contract N01-HD-6-2915 from the NICHD.