The body's reaction to mechanical disturbance is determined in part by the resultant stiffness of the joints. The long-term goals of this research are to understand the reflex and brainstem mechanisms which determine joint stiffness and which may function abnormally in disorders of movement. The stiffness of a joint depends upon the muscular stiffness of its agonists and antagonists. Muscular stiffness can, in turn, be partitioned into a component due to the mechanical properties of muscle and reflex component. The reflex component receives contributions from the same muscle synergists by way of autogenetic reflexes and from antagonists by way of non-antogenetic pathways. The analysis of reflex function proposed here is based on methods of evaluating these contributions to muscular stiffness. Mechanical measurements will be made on ankle flexors and extensors in decerebrate cats with intact midbrain structures. Net muscular stiffness will be calculated from measurements of changes in force in response to ramp length changes (K=dF/dL). Mechanical components will be estimated from the responses of electrically stimulated muscles and subtracted from net stiffness to give the reflex component. The magnitude of the reflex component of stiffness is an index of the net strength of transmission in the reflex pathways. Its measurement will be used to test the following hypotheses. 1) That the stretch reflex linearizes the mechanical properties of muscle or, equivalently, regulates its stiffness will be tested by studying muscles individually. 2) The hypothesis that Golgi tendon organs participate with muscle spindles in stiffness regulation will be tested by evaluating force feedback. 3) That the reflex component of a muscle in an intact joint system receives a contribution from non-autogenetic reflexes will be tested by comparing the result of stretching a muscle alone with the result of stretching the muscle and releasing its antagonist. 4) That signals from the brainstem can change or reset regulated stiffness by modulating transmission in reflex pathways will be tested by attempting to modulate stiffness using microstimulation of brainstem areas. If the regulated stiffness of a muscle can be reset, then the hypothesis that the strength of transmission in spinal reflexes is invariant and that resultant joint stiffness can be varied only by cocontraction would not be supported. If resetting exists, then some motor disorders may result from abnormalities of reflex function as well as from abnormal patterns of excitation of motoneuron pools.
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