1. The role of the catecholamine noradrenaline (NA) was examined during fictive swimming in Xenopus laevis tadpoles. 2. The primary effects of the amine in both embryonic and larval Xenopus was to markedly decrease motor frequency whilst simultaneously reducing rostrocaudal delays during swimming. 3. The NA-mediated modulation of swimming activity in Xenopus larvae can be reversed with phentolamine, a non-selective an adrenergic receptor antagonist, suggesting that NA may be acting through either ?1 or ?2 receptors, or a combination of both. 4. Intracellular recordings made from embryo spinal motorneurones revealed that reciprocal inhibitory glycinergic potentials are enhanced by NA. This effect is most prominent in caudal regions of the spinal cord where inhibitory synaptic drive is generally weaker. 5. NA was also found to enhance glycinergic reciprocal inhibition during swimming in larval spinal cord motomeurones. 6. Intracellular recordings, under tetrodotoxin, reveal that NA enhances the occurrence of spontaneous glycinergic inhibitory post synaptic potentials arising from the terminals of inhibitory intemeurones, suggesting that the amine is acting presynaptically to enhance evoked release of glycine during swimming. 7. The effects of NA on swimming frequency and rostrocaudal delay appear to be largely mediated through an enhancement of glycinergic reciprocal inhibition as blockade of glycine receptors with strychnine weakens the ability of the amine affect these parameters of motor output. 8. The effects of NA on motor output were also examined in embryos of the amphibian Rana temporaria. Whilst NA did not obviously affect swimming activity, the amine induced a non-rhythmic pattern of motor activity. 9. The free radical gas, nitric oxide also induced a non-rhythmic pattern of motor discharge that was remarkably similar to that elicited by NA, indicating that this neural messenger may be important for motor control.