1. The gastropyloric receptor (GPR) cells are stretch-sensitive muscle receptors in the crab stomatogastric nervous system that use both 5-hydroxytryptamine (serotonin) and acetylcholine as cotransmitters. Brief stimulation of these afferent neurons causes two gastric mill neurons to be recruited into the pyloric motor pattern. 2. The GPR cells evoke complex synaptic potentials in the lateral gastric (LG) and medial gastric (MG) motor neurons, two component neurons of the gastric mill central pattern generator. When the gastric mill is quiescent (as often happens in vivo), GPR stimulation transiently inhibits LG and MG. After this transient inhibition, these cells undergo a prolonged excitation during which they fire bursts of action potentials at a constant phase relation to the pyloric motor pattern. 3. To determine the causes for this effect, we examined the effects of GPR stimulation on these two cells and on the inferior cardiac motor neuron, which is electrically coupled to them. When GPR is stimulated, all three cells receive rapid biphasic synaptic potentials that are blocked by nicotinic antagonists, followed by a slow, prolonged depolarizing potential. 4. The slow, prolonged depolarizing potential is not blocked by nicotinic or muscarinic cholinergic antagonists but is mimicked and occluded by exogenously applied serotonin. 5. The prolonged excitation, mediated at least in part by serotonin, may be responsible for the recruitment of the gastric mill neurons into the pyloric motor pattern. Thus sensory input can directly exert prolonged modulatory effects that change the functional cellular composition of pattern-generating circuits.