The products of the fibrin clot hydrolysis performed by PC-12 cells modulated dose-dependently the rate of cell proliferation and favored their survival when seeded in suboptimal density. Co-incubation of PC-12 cells with fibrin degradation products enhanced cell adhesion to tissue culture plastic, as well as the number of nicotinic acetylcholine receptor alpha3 and alpha5 subunits expressed. It was demonstrated that, in fact, such a heterogeneous and comprehensive influence was a sum of effects exerted by different fibrin fragments. Low molecular weight fraction (below 30 kDa), but not a purified alphaC-domain, stimulated PC-12 cell proliferation, diminished their adhesion to plastic, increased nicotinic receptor expression and caused processes outgrowth. On the contrary, high molecular weight products, in particular D, DD and E fragments, enhanced PC-12 adhesion to plastic and, as a result, slowed cell division. Both high and low molecular weight fragments favored the survival of PC-12 cells. These results showed that fibrin degradation products support the vital functions of neuron-like cells, favor their contacts with extracellular surrounding and act as neurotrophic factors.