A&P Quiz 14

4. Describe the sequence of events involved in the contraction cycle of a skeletal muscle fiber.

1. Muscle contraction requires energy provided by the hydrolysis of ATP. Each myosin head contains both a site that binds to ATP and an ATPase enzyme that catalyzes the breakdown of ATP. When ATP binds to the myosin head, the ATPase in the myosin rapidly catalyzes the hydrolysis of ATP to ADP and a phosphate group (P). The energy liberated from ATP hydrolysis "cocks" the myosin head into its high-energy position, ready to work. The ADP and phosphate remain attached to the myosin head when it is cocked. 2. With the myosin head in its cocked position, The myosin head binds to actin. Resulting crossbridge is at about a 90° angle relative to the thick filament. 3. The power stroke occurs when the phosphate detaches from the myosin head and myosin pulls actin toward the center of the sarcomere; ADP leaves the myosin head at the end of the power stroke. The phosphate (inorganic phosphate, represented as Pi) detaches from the myosin head as it pivots on its hinge and moves from its cocked, high-energy position to its relaxed, lowenergy position. As the myosin pivots, it pulls the actin toward the center of the sarcomere. This action is known as the power stroke. Notice that the myosin crossbridge is now at about a 45° angle relative to the thick filament. At the end of the power stroke, ADP dissociates from the myosin head. 4. Another ATP binds to the myosin head, ATP breaks the attachment of myosin to actin.

Spasm

A muscle that is unable to relax. Common and may be due dehydration, electrolyte imbalances, muscle injury, or muscle overload. These spasms vary in degree, ranging from a "tight" muscle (also known as a muscle "knot") to a full spasm that impairs function and is typically very painful.

Chapter 10.4

Chapter 10.4

2. Describe the events at the neuromuscular junction that elicit an action potential in the muscle fiber.

Excitation Phase involves transmission of a signal from the motor neuron to the sarcolemma of a muscle fiber. Occurs at the neuromuscular junction (Figure 10.15): 1. An action potential from the brain or spinal cord arrives at the axon terminal and triggers Ca2+ channels in the axon terminal to open. 2. Calcium ion entry triggers exocytosis of synaptic vesicles. 4. ACh binds to ligand-gated ion channels in the motor end plate. 5. Ion channels open and Na+ enter the muscle fiber. 6. Entry of Na+ depolarizes the sarcolemma locally, producing an end-plate potential. Multiple end-plate potentials must be generated to produce a functional contraction of a muscle fiber. However, the ACh released from the synaptic vesicles is degraded and inactivated almost immediately by an enzyme in the synaptic cleft called acetylcholinesterase. For this reason, the neuron must continue to fire action potentials and release new ACh in order to stimulate repeated end-plate potentials in the muscle fiber.

3. Explain excitation-contraction coupling.

In this phase, the end-plate potential leads to an action potential in the sarcolemma, which in turn triggers events that result in contraction. 1. The end-plate potential spreads to the areas of the sarcolemma adjacent to the motor end plate. The change in voltage created by the end-plate potential opens enough voltage-gated sodium ion channels in the sarcolemma to stimulate an action potential. 2. The action potential is propagated like a wave along the sarcolemma, as depolarization of one area of the membrane triggers the next voltage-gated sodium ion channels to open continuing down the T-tubules. 3. On either side of a T-tubule is a terminal cisterna of the SR. that are directly linked to the T-tubules by voltage-gated proteins. T-tubule depolarization leads to the opening of calcium ion channels in the sarcoplasmic reticulum, and calcium ions enter the cytosol.

The synapse of a motor neuron with a muscle fiber

Neuromuscular Junction (NMJ)

The Big Picture

Page 361 Figure 10.20

Rigor Mortis

Progressive stiffening of skeletal muscles that begins about 3-4 hours after death, as the pumps that drive calcium ions back into the SR no longer have ATP to fuel their activity. As a result, calcium ions remain in the cytosol, where they bind with troponin and initiate a muscle contraction. The muscle fibers are unable to relax without ATP, so the myosin heads can't detach from actin. This causes the muscles to remain in spasm until the proteins in the myofilaments begin to degenerate, about 48-72 hours after death.

5. Explain the process of skeletal muscle fiber relaxation.

Three components: ACh release stops, the remaining ACh in the synaptic cleft is broken down, and the calcium ion concentration in the cytosol returns to its resting level. The sequence of events in relaxation is as follows (Figure 10.19): 1 ● Acetylcholinesterase degrades the remaining ACh, in the synaptic cleft into substances that can no longer stimulate the muscle. Without such stimulation, the ligand-gated ion channels in the motor end plate close, and the sarcolemma goes through, and the final repolarization occurs. 2 ● The sarcolemma returns to its resting membrane potential, and calcium ion channels in the SR close. The sarcolemma returns to its resting state once repolarization is complete. The calcium ion channels in the SR then close, so no further release of calcium ions from the SR takes place. 3 ● Calcium ions are pumped back into the SR, returning the calcium ion concentration in the cytosol to its resting level. Active transport pumps in the SR membrane consume ATP to pump calcium ions from the cytosol back into the SR. This activity decreases the calcium ion concentration of the cytosol, returning it to its resting level. 4 ● Troponin shifts and pulls tropomyosin back into position to block the active sites of actin, and the muscle relaxes. As the number of calcium ions in the cytosol returns to its resting level, calcium ions dissociate from troponin. This causes troponin to return to its original position, pushing tropomyosin back to where it blocks the active sites. This blocking prohibits the myosin heads from binding to actin, and the muscle contraction is over. The myofilaments then slide back into their original positions, with support from titin and other structural proteins.

1. Describe the anatomy of the neuromuscular junction.

Three parts: Fig 10.14 (1) The Axon Terminal: Found at the end of the axon contains synaptic vesicles that contain neurotransmitters like acetylcholine chemicals the neuron can release that trigger changes in its target cells. (2) Synaptic Cleft: narrow space between the axon terminal and the muscle fiber into which ACh is released. filled with collagen fibers and an extracellular gel that anchors the neuron in place and contains enzymes that break down ACh (3) Motor End Plate: Specialized region of the sarcolemma whose folded surface contains many receptors for ACh. A receptor is a protein within the plasma membrane that binds to a specific ligand. These receptors are actually ligand-gated ion channels; ACh is the ligand.

All skeletal muscle fibers are innervated

by motor neuron.

Each connection is known as a

synapse