Human short-latency reflexes show precise short-term gain adaptation after prior motion.

The central nervous system adapts the gain of short-latency reflex loops to changing conditions. Experiments on biomimetic robots showed that reflex modulation could substantially increase energy efficiency and stability of periodic motions if, unlike known mechanisms, the reflex modulation both acted precisely on the muscles involved and lasted after the motion. This study tests the presence of such a mechanism by having participants repeatedly rotate either their right elbow or shoulder joint before perturbing either joint. The results demonstrate a mechanism that modulates short-latency reflex gains after prior motion with joint-specific precision. Enhanced gains were observed hundreds of milliseconds after movement cessation, a timescale well suited to quickly adapt overall periodic motion cycles. A serotonin antagonist significantly decreased these postmovement gains diffusely across joints. But blocking serotonin did not affect the joint specificity of the gain scaling more than a placebo, suggesting that serotonin sets the overall reflex gain across joints after movement by an effect that is modulated in a joint-specific manner by an unidentified neural circuit. These results confirm the existence of a new, joint-specific, fast, persistent adaptation of short-latency reflex loops induced by motion in human arms. Our results expose a new spinal cord mechanism that modulates motoneuron gains, uniquely equipped to adapt movement in changing environments: it acts with joint-specific precision, reacts quickly to mechanical changes, and still persists long enough to accumulate information across movement cycles. The overall motoneuron gain across joints can be scaled down by an antagonist to serotonergic neuromodulation, whereas its joint specificity is unaffected by the antagonist and thus due to a complementary, unknown spinal mechanism.