The neuropeptide proctolin has distinguishable excitatory effects upon premotor cells and motorneurons of Homarus cardiac ganglion. Proctolin's excitation of the small, premotor, posterior cells is rapid in onset (5-10 s) and readily reversible (less than 3 min). Prolonged bursts in small cells often produce a "doublet" ganglionic burst mode via interactions with large motorneuron burst-generating driver potentials. In contrast to small cell response, proctolin's direct excitatory effects upon motorneuron are slow in onset (60-90 s to peak) and long-lasting (10-20 min). The latter include: a concentration-dependent (10(-9)-10(-7)M) depolarization of the somatic membrane potential; increases in burst frequency and enhancement of the rate of depolarization of the interburst pacemaker potential. Experiments on isolated large cells indicate: the slow depolarization is produced by a decrease in the resting GK and proctolin can produce or enhance motorneuron autorhythmicity . A two- tiered non-hierarchical network model is proposed. The differential pharmacodynamics exhibited by the two cell types accounts for the sequential modes of ganglionic burst activity produced by proctolin.