Nov 29, 2014

Controlling The Actin Myosin Interaction By Ca++ Ions

Muscle contraction is initiated by nerve impulse arriving at the neuromuscular junction. All the fibers innervated by a single motor neuron are a motor unit, and contract simultaneously in response to the action potential fired by the motor neurons. The sarcolemma of muscle fiber cell penetrates deep into the cell to form a hollow elongated tube the transverse tubule (T. tubule). Its lumen is continuous with the extra-cellular fluid. Thousands of T. tubule of each muscle cells are collectively called T-system.

Controlling The Actin Myosin Interaction By Ca++ Ions


It extends and encircles the myofibril at the level of Z line or A and I junction. The nerve impulse is carried through the T-tubule to the adjacent sarcoplasmic reticulum (SR). The calcium gates of the SR open releasing calcium into cytosol, binding of calcium ion to troponin molecules of the filament. The binding sites are exposed and cross bridges with myosin can form and contraction occurs.

The actin-myosin interaction is regulated by Ca++ ions in a process known as calcium-dependent regulation. In skeletal and cardiac muscle cells, Ca++ ions are released from the sarcoplasmic reticulum in response to an action potential. The rise in intracellular Ca++ levels then activates the interaction between actin and myosin, leading to muscle contraction.

In the absence of Ca++, the interaction between actin and myosin is weak and the muscle remains relaxed. When Ca++ ions bind to the regulatory protein troponin, which is located on the thin filaments of the sarcomere, it causes a conformational change in the troponin-tropomyosin complex, allowing the myosin heads to bind to actin.

Once the myosin heads are bound to actin, ATP hydrolysis occurs, leading to a conformational change in the myosin heads and a sliding of the thin filaments past the thick filaments. The amount of Ca++ present in the cytosol determines the strength of the actin-myosin interaction and the force generated by muscle contraction.

The importance of Ca++ ions in regulating the actin-myosin interaction can be seen in diseases such as malignant hyperthermia, in which excessive Ca++ release from the sarcoplasmic reticulum leads to uncontrolled muscle contractions and dangerous increases in body temperature. Additionally, drugs such as calcium channel blockers can be used to regulate the interaction between actin and myosin and reduce muscle contractility.

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