In the stomatogastric nervous system of the crab, Cancer borealis, a set of 4 serotonergic/cholinergic proprioceptive neurons, called gastropyloric receptor (GPR) cells, have effects on the pyloric motor pattern. In a semi-intact foregut preparation, the GPR cells are not activated by movements of the pyloric filter; instead they respond to the slower movements of the gastric mill (Katz et al., 1989). Thus, their activity is not synchronized to the pyloric motor pattern. However, when the GPR cells are stimulated in an in vitro preparation in a manner that resembles their normal firing pattern, they produce dramatic effects on the pyloric motor pattern. These effects include: (1) a prolonged increase in the pyloric cycle frequency, (2) a momentary pause in the motor pattern, (3) transient inhibition of some motor neurons, (4) strong excitation of other motor neurons, and (5) altered phase relationships of the different components of the motor pattern. These changes in the motor pattern are due to direct effects of the GPR cells on neurons in the pyloric central pattern generator (CPG). All of the cells in the pyloric circuit appear to receive GPR input. However, only 2 neurons receive detectable rapid nicotinic synaptic potentials. The other neurons receive only slower neuromodulatory input from GPR stimulation. The neuromodulatory effects include burst enhancement, plateau potential enhancement, excitation, and inhibition. These modulatory effects are largely mimicked by bath- applied serotonin (5-HT). Thus, primary sensory neurons can alter the production of motor patterns by a CPG through a phase-independent mechanism; these proprioceptors do not need to fire at a precise time in the cycle to be effective because their effects are mediated through the slower actions of the neuromodulator 5-HT.