Spasticity of the midline (axial) musculature may hinder (1) performing transfers, (2) efficient extremity and head movements, and (3) efficient respiration. Currently, gaps exist in our knowledge of the pathophysiology involved in spasticity development within the axial musculature. The goals of this study were (1) to study the effects of S(2) transection on the number and distribution of glutamatergic inputs, arising from primary afferents, and glycinergic inputs to sacrocaudal motoneurons; and (2) to correlate changes in these synaptic inputs with the development of spasticity within the tail musculature, which are the caudal counterparts to the trunk axial musculature. Animals with S(2) spinal transection were tested behaviorally using our established system. At 1, 2, 4, and 12 weeks post-injury, sacrocaudal motoneurons were retrogradely labeled with cholera toxin beta-subunit (CTB), and temporal changes in vesicular glutamate transporter 1 (VGLUT1) and glycine transporter 2 (GlyT2) inputs to CTB-labeled motoneurons were visualized using antibodies specific for each synaptic type and confocal microscopy. These time points correspond to each of 4 stages of spasticity development. There was no significant change in either VGLUT1 or GlyT2 labeling of sacrocaudal motoneurons at any of the time points examined. Spinal cord injury-induced spasticity, in the tail musculature, does not appear to involve either an increase in monosynaptic glutamatergic inputs from myelinated afferents or a decrease in glycinergic inputs to sacrocaudal motoneurons.