Evidence exists that the spinal cord is a glucocorticoid-responsive tissue, and glucocorticoids have beneficial effects in cases of spinal cord injury. Using sham-operated rats, spinal cord transected (TRX) rats, and TRX animals receiving dexamethasone (DEX) 5 min or 24 h post-lesion, we have examined the following GC-sensitive parameters 6 h after DEX treatment: (1) binding of glutamate to NMDA-sensitive receptors; (2) the activity of ornithine decarboxylase (ODC); and (3) levels of polyamines. We found that glutamate binding in the dorsal horn (Laminae 1-2) and central canal were upregulated in TRX rats, whereas DEX had an additional stimulatory effect. 24 h post-lesion, glutamate binding was unmodified in TRX or TRX+DEX rats. ODC activity was increased 10-fold in rats killed on the day of transection but only 2-fold 24 h post-lesion. DEX reduced ODC activity on transection day but highly increased it when given 24 h after surgery. The content of the polyamines spermidine and spermine were unchanged after TRX or DEX treatment, in contrast to putrescine which increased in TRX rats and further increased in TRX+DEX rats when measured the day post-lesion. Thus, parallel increases in ODC and putrescine 1 day after the lesion, suggest that glucocorticoid effects on growth responses due to polyamines may develop at a late period. The changes of glutamate binding in the dorsal horn and central canal due to early glucocorticoid treatment, further suggest hormonal modulation of neurotransmission in sensitive areas of the deafferented spinal cord.