Dysfunction of the spinal GABAergic system has been implicated in pain syndromes following spinal cord injury (SCI). Since lamina I is involved in nociceptive and thermal signaling, we characterized the effects of SCI on the cellular properties of its GABAergic neurons fluorescently-identified in spinal slices from GAD67-GFP transgenic mice. Whole-cell recordings were obtained from the lumbar cord of 13-17 day old mice, including those having had a thoracic segment (T8-11) removed 6-9 days prior to experiments. Following SCI, the distribution, incidence, and firing classes of GFP⁺ cells remained similar to controls, and there were minimal changes in membrane properties in cells that responded to current injection with a single spike. In contrast, cells displaying tonic/initial burst firing had more depolarized membrane potentials, increased steady-state outward currents, and increased spike heights. Moreover, higher firing frequencies and spontaneous plateau potentials were much more prevalent after SCI, and these changes occurred predominantly in cells displaying a tonic firing pattern. Persistent inward currents (PICs) were observed in a similar fraction of transect cells, and may have contributed to these plateaus. Persistent Na⁺ and L-type Ca²⁺ channels likely contributed to the currents, as both were identified pharmacologically. In conclusion, SCI induces a plastic response in a subpopulation of lamina I GABAergic interneurons. Alterations are directed toward amplifying neuronal responsiveness. How these changes alter spinal sensory integration and whether they contribute to sensory dysfunction remains to be elucidated.