Plasticity in Motoneurons Following Spinal Cord Injury in Fructose-induced Diabetic Rats.

Spinal cord injury (SCI) causes motor impairment and the proper excitation/inhibition balance in motoneurons is important for recovery. Diabetes mellitus impairs regenerative capacity following SCI. The purpose of this study was to assess the short-term plasticity (STP) of lumbar spinal cord motoneurons in conditions of (1) lateral hemisection (SCI), (2) fructose-induced diabetes (D), and (3) diabetes associated with hemisection (D + SCI). We show that in the cases of SCI, D, and D + SCI, the ratio of percentage share of excitatory and inhibitory combinations of motoneurons responses to high-frequence stimulation of sciatic nerve is multidirectional. In the SCI and D + SCI groups, the cumulative changes in generalized baseline frequencies decreased significantly. When we compared the cumulative changes in the intensity of excitatory and inhibitory responses relative to baseline during high-frequency stimulation (tetanization epoch), we found that there was a significant intensification in tetanic depression in the D + SCI groups versus SCI, as well as an intensification in tetanic potentiation in the D + SCI vs. D and D + SCI vs. SCI groups. Thus, in conditions of traumatic and/or metabolic pathology, the distinct synaptic inputs exhibit opposing plasticity for homeostatic control of neurotransmission and these integral changes most likely shape postsynaptic STP in the spinal motor network.