In rat embryonic sympathetic neurons from the superior cervical ganglia (SCG) NGF-mediated survival depends on the activation of the trkA receptor tyrosine kinase and on the activity of the intracellular plasmamembrane-anchored small G-protein p21ras. In contrast, chick sympathetic neurons derived from the more caudally located lumbosacral chain ganglia (LSCG) do not respond to activated p21ras (G12V-Ha-ras mutant). In these neurons endogenous p21ras and its downstream effector MAP kinase are activated but are not essential for NGF-dependent survival. Here we show that also in chick sympathetic neurons of the SCG permanently activated p21ras protein does promote neuron survival. Consistently, their NGF-mediated survival is sensitive to Fab fragments blocking endogenous p21ras activity. These results suggest that sympathetic neurons derived from sympathoenteric (SCG) and sympathoadrenal (LSCG) lineages differ in their requirement for p21ras in the NGF-mediated survival pathways.