Our previous studies have shown that extensive spinal lesions at T12 in the rabbit (ventral hemisection, VHS, or 3/4-section that spares one ventral quadrant, VQ) severely damaged the postural system. When tested on the platform periodically tilted in the frontal plane, VHS- and VQ-animals typically were not able to perform postural corrective movements by their hindlimbs, though EMG responses (correctly or incorrectly phased) could be observed. We attempted to restore postural control in VHS- and VQ-rabbits by applying serotoninergic and noradrenergic drugs to the spinal cord below the lesion through an intrathecal cannula. It was found that serotonin and quipazine (5-HT_1,2,3 agonist) did not re-establish postural corrective movements. However, when applied during ten-day period after lesion, these drugs produced a twofold increase of the proportion of correct EMG responses to tilts. It was also found that methoxamine (₁ noradrenergic agonist), as well as a mixture of methoxamine and quipazine, did not re-establish postural corrective movements, and did not increase the proportion of correct EMG responses. Serotonin (at later stages) and methoxamine induced periodical EMG bursts, suggesting activation of spinal rhythm-generating networks. Appearance of bursting seems to perturb normal operation of postural mechanisms, as suggested by methoxamine-induced abolishment of postural effects of quipazine. When applied in an intact animal, none of the tested drugs affected the value of postural corrections or evoked periodical bursting. We conclude that activation of the serotoninergic system (but not the noradrenergic one) causes selective enhancement of spinal postural reflexes during the earlier post-lesion period.