The activity of human muscle spindle endings in normal motor behavior.
In none of the above instances has the fusimotor system been found to be responsible for the described changes in stretch reflex gain. These findings do not prove that the fusimotor system is incapable of altering the gain of the stretch reflex; they do, however, establish that there are quite adequate mechanisms of gain control completely independent of the fusimotor system. One could reasonably question whether the fusimotor system ever operates primarily as a gain-controlling mechanism. That "more in" would probably result in "more out" cannot be disputed, but this may be of little real functional importance when compared with other possible sources of adaptive control of reflex activity. This conclusion has been reached by others in this department, working independently and using a quite different approach (79). Given that there are other adequate mechanisms of controlling reflex gain, one should question whether the fusimotor system plays any primary role in the disorders of stretch reflex gain that characterize spinal shock and cerebellar hypotonia on the one hand, and spasticity and Parkinsonian rigidity on the other hand.
D000344:Afferent Pathways / Q000502:physiology; D004576:Electromyography; D005071:Evoked Potentials; D006801:Humans; D007596:Joints / Q000294:innervation; D008465:Mechanoreceptors / Q000502:physiology; D009048:Motor Skills / Q000502:physiology*; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009470:Muscle Spindles / Q000502:physiology*; D009132:Muscles / Q000294:innervation; D010543:Peroneal Nerve / Q000502:physiology; D012018:Reflex / Q000502:physiology