Although neural plasticity has traditionally been studied within the brain, evidence indicates that the spinal cord is quite plastic as well. Spinal neurons can even support a simple form of instrumental learning (Grau et al., 1998), as indicated by spinally transected rats’ ability to exhibit an increase in hind limb flexion duration when limb extension is associated with shock (controllable shock). If limb extension is not associated with shock (uncontrollable shock), a learning deficit develops. Recent research indicates that other forms of plasticity, such as long-term potentiation and central sensitization, do not depend on neural activity alone, but also on glial cells. I examined whether glial cells are also necessary in spinal instrumental learning and the learning deficit. Therefore, two glial inhibitors were selected: minocycline and fluorocitrate. To examine the role of glial cells in spinal instrumental learning, rats received intrathecal minocycline, fluorocitrate, or saline prior to testing with 30-minutes of controllable leg-shock. Results indicate that both drugs dose-dependently reduced acquisition, with higher doses resulting in shorter response durations. Once the response was acquired, fluorocitrate did not alter response maintenance. This suggests that glial cells are involved in the acquisition, but not the maintenance, of spinal learning. To examine the role of glial cells in the spinal learning deficit rats were given intrathecal minocycline, fluorocitrate, or saline prior to testing with 6-minutes of uncontrollable tail shock or no shock. Twenty-four hours later all rats were tested with 30-minutes of controllable leg-shock. Results indicated the learning deficit induced by uncontrollable shock was prevented by prior administration of fluorocitrate. Minocycline did not prevent the deficit; moreover, it appears that even in the absence of shock, minocycline caused a learning deficit. Overall, this data indicate that glial cells are necessary for the acquisition of spinal instrumental learning and the learning deficit. Furthermore, it provides further evidence for the role of glial cells in plasticity.