Migration of neuronal cell bodies from their birthplace to their final destination is a crucial step in brain development. Proper organization and function of neurons circuits depends on developmental processes such as neuronal specification and migration, axon guidance and maturation of synapses. Improper neuronal migration may play a role in human diseases such as schizophrenia, mental retardation, and autism. Despite its importance, the consequences of abnormal neuronal migration on circuit organization and behavioral function are poorly understood. To investigate migration of neurons we study the facial branchiomotor (FBM) neurons in zebrafish as a model system. In the zebrafish hindbrain, FBM neurons migrate caudally in the hindbrain from rhombomere 4 to their final destination rhombomeres 6/7, and innervate jaw and gill muscles. In order to examine the behavioral consequences of defective migration in FBM neurons, we characterized the maturation and function of the neural circuits controlling jaw movement in zebrafish larvae between 3-7 days post fertilization (dpf) by time-lapse imaging and quantitative analysis. At 3 dpf larvae exhibited little or no jaw movement and minimal gape activity (opening and closing of the lower jaw). At 5 dpf, larvae exhibited rhythmic jaw movements such that gape increases in amplitude and frequency. By 7 dpf jaw movement are very robust and rapid, with a doubling of frequency over 5 dpf larvae. These data indicate that jaw movements develop and mature between 3- 7 dpf, 24-36 hours after FBM neurons have completed caudal migration and 72 hours after completed axon projection to the jaw muscle. To study the consequences of defective neuronal migration, we measured the gape activity of off limits (fzd3a-/-) mutant larvae where FBM neurons fail to migrate out of rhombomere 4. Mutant larvae exhibited a small increase in gape activity from 3-7 dpf, resulting in very low gape frequency at 5 and 7 dpf compared to wild type siblings. These data suggest that a failure of FBM neuron migration leads to defects in motor circuits, resulting in a failure of jaw movement to be established properly. Given the defects in jaw movements in off limits mutants, we wondered whether another functional output of the branchiomotor circuits, namely food intake, was also affected in mutants. As expected, olt mutants exhibited a significant decrease in food intake. These results demonstrate that misslocation of the FBM neurons can lead to deficits in the functional output of the branchiomotor circuits. Our studies establish a foundation for dissecting the neural circuits driving a motor behavior essential for survival.