Most vertebrate locomotion central pattern generators (CPG) are presumed to include excitatory interneurons which provide the excitatory drive for the rhythm-generating circuit. However, only in the lamprey have these interneurons been well defined with physiological and anatomical evidence (Parker, 2003). In the Xenopus tadpole spinal swimming circuit, a group of interneurons with ipsilateral descending axons (dIN) were proposed to provide glutamatergic excitation to spinal neurons during swimming (Dale and Roberts, 1985). Due to the difficulties in making intracellular paired recordings with sharp electrodes and cell labelling with horseradish peroxidase, the evidence on the anatomical identity of these neurons was very limited. The application of whole-cell patch recording techniques has greatly eased these difficulties (Li et al., 2002) and this issue is revisited in this study. Means are given with their SDs. Recordings were made using stage 37/38 Xenopus tadpoles immobilised with 10 μM α-bungarotoxin. Paired recordings were made with whole-cell recording pipettes and neuron anatomy was revealed after neurobiotin filling. Results showed that dINs with descending ipsilateral axons directly excited more caudal CPG neurons of all types. These included: motorneurons (n = 24/28 pairs); commissural reciprocal inhibitory neurons (n = 4/4); ascending neurons, providing negative feedback to the sensory pathway and CPG (n=3/4); and other dINs (n=34/40). The unitary EPSPs produced by dIN impulses were often large (mean max amplitude 13.1 ± 1.7 mV; n = 10 pairs). Their latencies were short and consistent (1.32 ± 0.10 ms; n = 10 pairs) and neurobiotin staining also revealed close contacts between descending dIN axons and the postsynaptic neuronal dendrites or somata, suggesting these interactions are mono-synaptic (Li et al., 2002). During swimming dINs fired reliably and their spikes appeared earlier during each cycle than other CPG neurons at similar longitudinal locations (t-test, 16 dINs, 12 CPG neurons, p<0.05), suggesting that dINs are the source of the excitation that normally drives swimming. These new results confirm an excitatory role for dINs in tadpole swimming.