Plasticity is an intrinsic reaction to adapt to environmental pressures, physiologic changes, and experiences. Although plasticity is most studied in brain, it is also evident in the spinal cord. Spinal plasticity is associated with the functional recovery of several neurological disorders. However, spinal plasticity may also lead to sequelae of neurological disorders, e.g. spasticity, which is one of the most common sequelae of SCIs and strokes. Hence, it is worthwhile developing non-invasive protocols to modulate plasticity in the human spinal cord for exploring the underlying mechanism and the therapeutic approach of relevant disorders. The aim of the study was to develop electrical stimulation protocols based on theta burst stimulation (TBS) for the induction of spinal plasticity in humans. We tested electrical median nerve stimulation in the pattern of continuous TBS (spinal cTBS) at different stimulus intensity and duration on eight healthy subjects. The ratio of the amplitude of H-reflex to maximum M wave (H/M ratio) was measured before and after spinal cTBS for its effect on spinal plasticity. Moreover, short-interval intracortical inhibition and intracortical facilitation (SICI/ICF) and spinal reciprocal inhibition (RI) were tested to clarify the underlying mechanisms of spinal cTBS applied to the median nerve. At 90% of H-reflex threshold, spinal cTBS for 80 s (cTBS1200) significantly suppressed H/M ratio for 45 min or more, while spinal cTBS for 40 s (cTBS600) only showed inhibition at 30 min after the end of spinal cTBS. Increasing the stimulus intensity to 110% threshold did not enhance the suppression effect, but, in contrast, produced a facilitatory effect. On the other hand, spinal cTBS at 80% threshold may be too weak to activate the spinal circuits to produce any effect on the H/M ratio. Maximum M wave remained unchanged after all tested spinal cTBS protocols, suggesting that the excitability of the anterior horn cell and its axon was not modified by spinal cTBS. The MEP size, SICI/ICF and RI were not changed by cTBS1200 at 90% threshold when the H/M ratio was suppressed further confirmed that the effect of spinal cTBS was very likely happening at the monosynapse of H-reflex at the spinal level. Spinal cTBS has shown the ability to modulate the amount of H-reflex at the spinal level. The modulation effect is very likely due the change of the efficiency of the monosynapse within the loop though plasticity-like mechanism. Moreover, the effect of spinal cTBS depends on the stimulus intensity and duration. In the future, we expect to apply the current protocol to patients with, for instance, spasticity to evaluate plasticity phenomena in the spinal cord and to test the therapeutic potential of the protocol. This work was supported by National Institutes of Health and National Science Council of Taiwan and Chang Gung Memorial Hospital. We would like to thank Su-Juan Lin for the assistance in conducting the experiments.