Abstract

One component of the dynamic response of muscle spindles is characterized by a phase lead and frequency dependent sensitivity in response to sinusoidal stretches at frequencies around 1 Hz. Possible mechanisms producing this component, designated the "mid-frequency" dynamics, were investigated by testing the hypotheses that they arise from the mechanical behavior of the intrafusal muscle and alternatively from within the sensory terminals. Destruction of the myofibrillar structure of the intrafusal muscle fibers did not alter the mid-frequency dynamics, indicating that they do not arise from viscoelastic properties of the intrafusal muscle. An Arrhenius plot of the temperature dependence of the mid-frequency dynamics yielded an equivalent activation energy of 6.5 Kcal/M in the temperature range 23-42 degrees C and a 3-fold higher activation energy at lower temperatures. These observations are consistent with a dynamic process associated with a membrane-bound biochemical process. The addition of Ca++ and Ca(++)-activated-K+ (K(Ca] channel blockers (ZnCl2, Apamin and TEA) to the bathing solution altered the response dynamics by reducing the mid-frequency phase lead. The results suggest a negative feedback on the membrane potential generated by K+ efflux following a Ca++ influx that opens K(Ca) channels. A quantitative model fit to the experimental data yields a time constant of about 80 ms representing the limiting process associated with activation of the K(Ca) channels in this system. The results indicate that the mechanism underlying the mid-frequency dynamics includes at least two processes: one, not identified in this study, generates the phase lead and another, involving Ca++ and K(Ca) channels, provides a negative feedback that modifies the phase lead.

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