(A) Drawing of the optical fiber implant above the sacral spinal cord (upper panel). (B) Gross EMG recordings from tail muscles in acutely (black trace) and chronically spinalized (red trace) Vglut2Cre; R26ChR2 mice during light stimulation of the first coccygeal segment of the spinal cord (train of 15 pulses, 20 ms, 10 Hz). Stimulation of excitatory interneurons (eINs) in chronically spinalized mice always generated spasms (4 out of 4). See also Video 4. (C) Co3 ventral root recordings in isolated spinal cord from a chronically spinal cord transected Vglut2Cre; R26ChR2 mouse during optogenetic stimulation at the third coccygeal segment of the spinal cord (train of 15 pulses, 20 ms, 10 Hz, upper trace), after application of 10 μM of the GABAA antagonist picrotoxin in combination with 1 μM of the glycinergic antagonist strychnine (middle trace), and after application of a broad range glutamatergic antagonist, Kynurenic acid (0.5 mM, lower trace). (D–F) Schematics of the in vitro experiments with indication of dorsal root stimulation (DRS), ventral rootlets recordings and optical stimulation in chronically spinal cord transected Vglut2Cre; eNpHR3 (D, N = 5), VIAATCre; R26ChR2 (E, N = 10), and VIAATCre; eNpHR3 (F, N = 10) mice. Raw ventral root recordings with only optogenetic stimulation (DI–FI), only electric stimulation (DII–DII), simultaneous optogenetic and electric stimulation (DIII–FIII) and optogenetic stimulation delayed in time (DIV-FIV). Note that optogenetic activation of iINs (EI) does not evoke spasms while their activation during a spasm immediately terminates it (Eiii). Insets in DII–III show that the monosynaptic and polysynaptic inputs to motor neurons are similar with and without optogenetic stimulation during the electrical stimulation.