Nerve injury in newborn animals results in the loss of motoneurons and dorsal root ganglion neurons and long-term changes in reflex activation of surviving motoneurons. Parvalbumin has been previously shown to be found in large-diameter primary afferent axons and interneurons in the spinal cord, and was used here to study the changes in parvalbumin-immunoreactive appositions onto identified tibialis anterior/extensor digitorum longus (TA/EDL) motoneurons, during both normal development and following neonatal nerve injury in the rat spinal cord. During normal development, there was a decrease in the number of parvalbumin-immunoreactive appositions onto TA/EDL motoneurons. Thus, at postnatal day 7 (P7), there were 72.8 ± 17.5 (mean ± SD) appositions per motoneuron and by P14, it had decreased to 38.8 ± 13.2 (mean ± SD; p > 0.05). Following neonatal nerve injury at P2, there were fewer parvalbumin-positive afferent appositions close to the TA/EDL motoneurons than normal, so that at P7, there were 53.5 ± 17.1 (mean ± SD), and at P14, it further decreased to 25.8 ± 8.6 (mean ± SD; p > 0.05). This injury-induced reduction in the number of parvalbumin-immunoreactive boutons apposing TA/EDL motoneurons may result, at least in part, from the death of dorsal root ganglion cells with the consequent loss of their central projections. The alterations in the number of parvalbumin-positive appositions close to motoneurons observed in this study may contribute to the changes in the pattern of reflex activity observed in the developing spinal cord both during normal development and following neonatal injury.