This paper analyzes the effects of exogenously supplied GM1 on the development, i.e., specific neurotransmitter uptake capability and survival, of the dopaminergic neurons present in fetal mouse-dissociated mesencephalic cells. Exogenous GM1, but not asialo-GM1, sialic acid, or the oligosaccharide chain of GM1, enhances in a time- and concentration-dependent manner the specific 3H-dopamine uptake (increase of the apparent Vmax and decrease of the apparent Km value) and the long-term survival of the dopaminergic neurons. The GM1 effects on the behavior of the dopaminergic neurons require the presence of cell-derived neuronotrophic influences present within the culture system and are associated with an increase in the response of the cells to the trophic influences. GM1 effects are not limited to dopaminergic neurons, and depend on the stable association of the ganglioside molecule with the cells. It is suggested that GM1 is not a trophic agent per se, but rather potentiates neuronotrophic activities and/or exerts independent influences to which neurons respond only if appropriately supported.