Skip to main content
. 1998 Feb 23;140(4):911–923. doi: 10.1083/jcb.140.4.911

Figure 4.

Figure 4

(A) The p75NTR antibody, REX, inhibits the BDNF-mediated apoptosis of sympathetic neurons. A comparison of sympathetic neuron survival, as monitored using MTT assays, in response to 25 mM KCl ± BDNF with and without the presence of the function-blocking anti-p75NTR, REX. Sympathetic neurons were cultured in 50 ng/ml NGF for 5 d, washed free of neurotrophin-containing medium, and then incubated for 2 d in 25 mM KCl or 25 mM KCl + 100 ng/ml BDNF with or without REX. Results of two representative experiments, each of which was performed in triplicate, are shown. In all cases, results represent the mean ± standard error, and are normalized so that the survival mediated by 25 mM KCl alone is 100%. REX by itself had no significant effect (P > 0.05) on sympathetic neuron survival as mediated by 25 mM KCl. (***P < 0.004 for the comparison between 25 mM KCl + REX and 25 mM KCL + 100 ng/ml BDNF + REX). (B) Death of cultured p75NTR−/− neurons is delayed after NGF withdrawal. Time course of survival of cultured p75NTR−/− and p75NTR+/+ (Control) neurons following NGF withdrawal. Representative fields of neurons were counted immediately upon NGF withdrawal, and again every 24 h. Results are normalized so that the number of neurons at the time of NGF withdrawal is 100%. Results represent the mean ± standard error of the combined data from five individual experiments each for the p75NTR−/− and control neurons; every individual experiment was performed in triplicate. (***P < 0.002 for the comparison between p75NTR−/− and control neurons at each time point).