The pathway mediating the monosynaptic stretch reflex has served as an impo
rtant model system fur studies of plasticity in the spinal cord. Its useful
ness is extended by evidence that neurotrophins, particularly neurotrophin-
3 (NT-3), which has been shown to promote spinal axon elongation, can modul
ate the efficacy of the muscle spindle-motoneurone connection both after pe
ripheral nerve injury and during development. The findings summarized here
emphasize the potential for neurotrophins to modify function of both damage
d and undamaged neurones. It is important to recognize that these effects m
ay be functionally detrimental as well as beneficial.