MB 15 (Ch. 50)
Sarcomere action potentional
When an action potential causes the Ca2+ level to rise in the sarcomere, the cycle of myosin-actin interactions begins with binding of the myosin heads to actin. Binding of actin is followed by the power stroke, which pulls the thin filament toward the center of the sarcomere. When the myosin head binds ATP, it detaches from actin. Then, the myosin head hydrolyzes ATP to ADP and Pi, which extends the myosin head and puts it in position to bind actin once again. The cycle continues as long as Ca2+ is present in the sarcomere. The result of repeated cycles is the shortening of the sarcomere, and ultimately, contraction of the muscle.
The muscle cell and its motor neuron
Skeletal muscle consists of many bundles of fibers that run the entire length of the muscle. Each fiber is an individual muscle cell. Each muscle cell is in contact with a single motor neuron that controls the contraction of that cell. The diagram below shows a single muscle fiber and its motor neuron. Understanding the unique structural components of a muscle cell and its interaction with its motor neuron is a prerequisite for understanding muscle contraction and how it is regulated. [A skeletal muscle cell is composed of a large number of contractile fibrils called myofibrils. The basic unit of contraction in a myofibril is a sarcomere. The sarcomeres are arranged end to end along the entire length of each myofibril. Each myofibril is partially surrounded by a specialized form of endoplasmic reticulum, called the sarcoplasmic reticulum. An action potential traveling along the motor neuron initiates an action potential in the muscle cell, which leads to muscle contraction. At the synaptic terminal of the motor neuron, an action potential causes the release of neurotransmitters, which subsequently trigger an action potential on the plasma membrane of the muscle cell. This action potential is propagated deep into the muscle cell via the T (transverse) tubules. In the interior of the cell, the action potential initiates changes in the sarcoplasmic reticulum.]
The role of T tubules in conducting an action potential
Propagation of an action potential in a skeletal muscle cell links the signal from a motor neuron to contraction of the muscle cell. An action potential in a muscle cell is propagated by the same mechanism as in neurons, the sequential opening and closing of voltage-gated Na+ and K+ channels in the plasma membrane. However, in muscle cells, the topography of the plasma membrane is quite different than in neurons, and this difference is critical to the function of muscle cells. Which of the following statements correctly describe(s) T tubules and their role in conducting action potentials in muscle cells? A- -T tubules carry action potentials into the interior of the muscle cell via voltage-gated Na+ and K+channels. -Without T tubules, the muscle cell would not be able to contract. -T tubules are infoldings of the plasma membrane that encircle the myofibrils and are in contact with the sarcoplasmic reticulum. [The T tubules are invaginations of the muscle cell plasma membrane that extend deep into the muscle cell and are in close contact with (but not continuous with) the sarcoplasmic reticulum. The T tubules play two important roles in linking an action potential to muscle contraction. T tubules propagate the action potential from the plasma membrane into the interior of the muscle cell via voltage-gated Na+ and K+ channels. An action potential carried by a T tubule regulates the opening and closing of Ca2+ channels in the sarcoplasmic reticulum. The resulting change in cytosolic Ca2+ concentration triggers contraction of the myofibrils.]
How an action potential affects Ca2+ movement in a muscle cell
The sarcoplasmic reticulum is a specialized form of ER that surrounds each myofibril. The sarcoplasmic reticulum functions to control cytosolic Ca2+ levels in the muscle cell. Changes in cytosolic Ca2+ concentrations couple action potentials to muscle contraction. The concentration of Ca2+ ions in the sarcoplasmic reticulum is typically much higher than the Ca2+ concentration in the cytosol. This concentration gradient is key to the movement of Ca2+ in the muscle cell in response to an action potential. The cycle diagram below shows the sequence of events that affect Ca2+ levels in a muscle cell, beginning with the propagation of an action potential down a T tubule (top of the diagram). [In muscle cells, the cytosolic Ca2+ concentration is kept low by active transport of Ca2+ from the cytosol into the sarcoplasmic reticulum. When an action potential moves down the T tubules, it triggers Ca2+ channels in the sarcoplasmic reticulum to open. As a result, Ca2+ ions rush into the cytosol. Once in the cytosol, the Ca2+ ions diffuse into the myofibrils, where they enable muscle contraction to begin. When the action potential is completed, the Ca2+ channels in the sarcoplasmic reticulum close, and Ca2+ ions are again pumped back into the sarcoplasmic reticulum. As the cytosolic level of Ca2+ drops, Ca2+ ions diffuse out of the myofibrils, stopping muscle contraction.]
Structure of the sarcomere
The thin filaments and thick filaments and their associated proteins are the key functional components of the sarcomere. It is important to be able to identify these components in order to understand their roles in muscle contraction.
Structure of the sarcomere cont. process
The thin filaments and thick filaments in a sarcomere interact with each other when an action potential triggers the muscle to contract. The thin filament is composed of actin and regulatory proteins that respond to changes in the Ca2+ concentration in the sarcomere. The thick filament is composed of myosin proteins, whose heads bind to actin and pull the thin filament toward the center of the sarcomere.
