Noradrenaline (NA) is a potent modulator of locomotion in many vertebrate nervous systems. When Xenopus tadpoles swim, waves of motor neuron activity alternate across the body and propagate along it with a brief rostro-caudal delay (RC-delay) between segments. We have now investigated the mechanisms underlying the reduction of RC-delay s by NA. When recording from motor neurons caudal to the twelfth postotic cleft, the mid-cycle inhibition was weak and sometimes absent, compared to more rostral locations. NA enhanced and even unmasked inhibition in these caudal neurons and enhanced inhibition in rostral neurons, but to a lesser extent. Consequently, the relative increase in the amplitude of the inhibition was greater in caudal neurons, thus reducing the RC-inhibitory gradient. We next investigated whether NA might affect the electrical properties of neurons, such that enhanced inhibition under NA might promote postinhibitory rebound firing. The synaptic inputs during swimming were simulated using a sustained positive current, superimposed upon which were brief negative currents. When these conditions were held constant NA enhanced the probability of rebound firing--indicating a direct effect on membrane properties--in addition to any indirect effect of enhanced inhibition. We propose that NA preferentially enhances weak caudal inhibition, reducing the inhibitory gradient along the cord. This effect on inhibitory synaptic transmission, comprising parallel pre- and postsynaptic components, will preferentially facilitate rebound firing in caudal neurons, advancing their firing relative to more rostral neurons, whilst additionally increasing the networks ability to sustain the longer cycle periods under NA.