Poster (Knowledge Generation) ID 1985240

Following a spinal cord injury, there is a significant loss of monoamines below the lesion. In the rat model, exogenous administration of the serotonin precursor, 5-hydroxytryptophan (5HTP), increases neural excitability through augmentation of spinal serotonin levels. To determine whether this compensatory mechanism can be harnessed to restore serotonergic modulation in humans after SCI, participants visited the lab on four occasions where they received i) placebo, ii) carbidopa, iii) 50mg 5HTP+carbidopa, or iv) 100mg 5HTP+carbidopa in a randomized, crossover design. Cutaneomuscular reflexes (CMR) were obtained pre-drug and 30, 60, 90 and 120-min post-drug intake. Surface electromyography was also recorded during a pedalling movement pre- and post-drug. Nine participants with chronic, complete SCI (35.3±5.5 years) and four participants with chronic, incomplete SCI (47.0±19.7years) were enrolled. Following ingestion of 100mg 5HTP only, the short polysynaptic and long-lasting reflex components of the CMR were significantly increased by ∼ 86±61% and 58±17% respectively in individuals with complete SCI. No significant changes were noted in the cohort of individuals with incomplete SCI. Integrated EMG during pedalling was increased in multiple lower extremity muscles during the extension and flexion phases of the cycle following both 50-mg (82±15% and 51±7%) and 100-mg 5HTP (140±27% and 130±16%) in individuals with more severe injuries, but not in those with incomplete injuries. Ingestion of 5HTP facilitates neural excitability and induces rhythmic muscle activity in previously inactive muscles during an assisted pedalling movement in individuals with chronic, complete SCI. This has significant clinical implications for rehabilitation after SCI.