A subpopulation of calbindin-immunoreactive neurons in lamina VII of the spinal cord has been identified by its location as Renshaw cells, the anatomical substrate for recurrent inhibition. The expression of calbindin (28 kDa) in these calbindin-containing rat ventral horn interneurons was studied with immunocytochemistry after sciatic nerve injuries. One week after axotomy calbindin immunoreactivity was strongly reduced on the lesioned side between levels L4 and L6, while calbindin-containing neurons and fibers were still numerous contralaterally and cranially to the lesioned levels. With the progression of regeneration, calbindin-immunoreactive neurons reappeared, reaching a normal distribution 6-8 weeks after the crush. Similar changes could be mimicked by the intramuscular administration of botulinum toxin. These results suggest that calbindin expression in putative Renshaw cells of the spinal cord might be functionally responsive and that maintenance of calbindin expression may depend on the integrity of motoneurons and neuromuscular transmission.