?/1 pt Mutations in skeletal muscle proteins can have profound impacts on muscle

Question

?/1 pt Mutations in skeletal muscle proteins can have profound impacts on muscle function. You are working with a frog leg preparation that has a mutation in its Ca2+ ATP-ase. This mutation enhances the ability of the Ca2+ ATP-ase to sequester Ca2+ into the Sarcoplasmic Reticulum. It works so well that virtually ALL the Ca2+ released by the Sarcoplasmic Reticulum is re-sequestered immediately. You attempt to perform the tetany experiment on this preparation as you did in the frog lab. A. Clearly (but briefly) explain the mechanism by which tetany normally produces changes in muscle tension. How would it be different for the mutated frog? B. Draw your expected results for the tetany experiment for BOTH a NORMAL frog and your mutated one.

Explanation / Answer

A. ans:Tetanic contraction is defined as a sustained muscle contraction exhibitted when the motor nerve ,upon innervating a skeletal muscle emits action potentials at a very high rate.During this state, a motor unit that has been optimally stimulated by its motor neuron sustains the stimulation for some time. This occurs when a muscle's motor unit is stimulated by multiple impulses at sufficiently high frequency. Each stimulus causes a twitch. If stimuli are delivered slowly enough, the tension in the muscle relaxes between successive twitches. High frequency stimuli cause the twitches to overlap, resulting in tetanic contraction.

It takes about 10 msec for an action potential to propagate across the length of a skeletal muscle fiber in the frog gastrocnemius, whereas the total time for a twitch contraction of the gastrocnemius may be ~150 msec. Thus, many action potentials can occur in the amount of time needed for a single twitch. If a muscle relaxing from contraction is stimulated before it fully relaxes, the sarcoplasmic reticulum releases more Ca2+, and the cell begins to contract again without fully relaxing. As an aftereffect, the twitches are partially fused together. If stimulated at progressively at higher frequency, the amount of relaxation inbetween twitches is considerably reduced till a steady state of tetany is generated.Upon muscle contraction,the elastic elements are fully stretched and more tension is exerted directly on the attachments.The muscle fibers undergo action potentials as Ca2+ is released from the sarcoplasmic reticulum. If the sarcoplasmic reticulum is induced by another action potential to release Ca2+ before it has fully recovered all of the Ca2+previously released, then there will be overall more Ca2+ in the cytosol during the second contraction, more interaction between actin and myosin, and a stronger resultant contraction.

Myocardial contraction and relaxation are dependent upon the rise and fall of cytosolic Ca2+] in cardiac myocytes. The release and sequestration of Ca2+ by the sarcoplasmic reticulum are the principal mechanisms through which this occurs. During relaxation, Ca2+ is actively transported from the cytosol into the sarcoplasmic reticulum; during contraction, this sequestered Ca2+ is passively released into the cytosol through ryanodine-sensitive Ca2+ channels.Because of the dependence of contraction and relaxation upon ATP-dependent Ca2+ sequestration by the sarcoplasmic reticulum, the possibility that an impairment in this process contributes to heart failure. In case of the mutated organism(frog) mutation of the ATPasethat results in resequestration of all the available Ca2+ will be fatal .

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