In the nervous system, apoptosis is a major process during embryonic and postnatal stages. In chick, experimental cell death can be obtained by axotomy. We have compared the responses of olfactory neurons to axotomy at embryonic stage E17 and postnatal stages.Forty-three chicken embryos and 32 young chickens less than 3 weeks old were used. We combined optic microscopy, electronic microscopy, terminal (TdT)-mediated dUTP-nick end labeling (TUNEL) method and gel electrophoresis of genomic DNA to analyze cell death. Cells in synthetic phase were labeled by bromodeoxyuridine injected i.p. and detected by immunohistochemistry. Apoptotic index and 5-bromo-2'-deoxyuridine (BrdU) labeling index were calculated for each stage. The Wilcoxon test was used for statistical analysis. A P value <0.05 was considered significant. Within 3 days following axotomy in E17 chicken embryos, there was no significant increase of apoptosis on the lesion side analyzed 3, 6, 12, 18, 24, 48 or 56 h later. A slight increase of bromodeoxyuridine incorporation appeared at 3 h, was weakly significant at 24 h (P=0.045) and the return to basal rate took place at 48 h. In postnatal stages, an apoptotic wave appeared 12 h after axotomy, reached a maximum at 24 h, and then decreased between 48 h and 72 h. A significant elevation of bromodeoxyuridine incorporation occurred on 48 h with a 24 h delay after the peak of apoptotic death. This differential response to axotomy in embryos and postnatal chickens might be due to a less complete maturation and higher plasticity of embryonic olfactory neurons corresponding to different requirement for survival and differentiation factors. Thus the embryonic or immature neurons would depend more on local epithelial environment and mature or postnatal neurons would require target-derived survival factors and die from apoptosis after their shortage resulting from axotomy.