Excitation-contraction coupling is the process by which a potential for muscle action in the muscle fiber causes the myofibrils to contract. [20] In skeletal muscle, excitation-contraction coupling is based on direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as ryanodine 1 receptor, RYR1) and voltage-controlled L-type calcium channels (identified as dihydropyridine receptors, DHPR). DHPR are located on the sarcolemma (which includes the surface sarcolemma and transverse tubules), while RyRs are located across the SR membrane. The narrow arrangement of a transverse tubule and two SR regions containing RyRs is described as a triad and is primarily the place where the excitation-contraction coupling takes place. Excitation-contraction coupling occurs when depolarization of the skeletal muscle cell leads to a muscle action potential that spreads through the cell surface and into the tubular T network of the muscle fiber, thereby depolarizing the inner part of the muscle fiber. Depolarization of the internal parts activates dihydropyridine receptors in terminal cisterns, which are located near ryanodine receptors in the adjacent sarcoplasmic reticulum. Activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (with conformational changes that activate ryanodine receptors allosterically). When the ryanodine receptors open, Ca2+ is released from the sarcoplasmic reticulum into the local connection space and diffuses into the bulk cytoplasm to cause a spark of calcium. Note that the sarcoplasmic reticulum has a high calcium buffering capacity, which is partly due to a calcium-binding protein called calequesterin. The almost synchronous activation of thousands of calcium sparks by the action potential causes an increase in calcium at the cell level, which leads to the increase in calcium transient. The Ca2+ released in the cytosol binds to troponin C through the actin filaments to allow the transverse bridge cycle, which generates strength and movement in certain situations. Calcium ATPase of the endoplasmic sarco/reticulum (SERCA) actively pumps Ca2+ into the sarcoplasmic reticulum.
When Ca2+ falls back to the level of rest, strength decreases and relaxation occurs. Figure 6.7. When (a) a sarcomere (b) contracts, the Z lines move closer together and the I band becomes smaller. The A-band remains the same width and at full contraction the thin filaments overlap. The movements of myosin seem to be a kind of molecular dance. Myosin moves forward, binds to actin, contracts, releases actin, and then moves forward again to bind actin in a new cycle. This process is called the myosin-actin cycle. Since the segment of myosin S1 binds and releases actin, it forms so-called transverse bridges that extend from thick myosin filaments to thin actin filaments. The contraction of the S1 region of myosin is called a power stroke (Figure 3). The power stroke requires the hydrolysis of ATP, which breaks a high-energy phosphate bond to release energy.
When a muscle is at rest, actin and myosin are separated. To prevent actin from binding to the active center of myosin, regulatory proteins block molecular binding sites. Tropomyosin blocks myosin binding sites to actin molecules, prevents the formation of transverse bridges, and prevents contraction in a muscle without nerve input. Troponin binds to tropomyosin and helps position it on the actin molecule; It also binds calcium ions. Cytoplasmic calcium binds to troponin C and moves the tropomyosin complex from the actin binding site so that the myosin head can bind to the actin filament. From this point on, the contractile mechanism is essentially the same as in skeletal muscle (above). In short, using ATP hydrolysis, the myosin head pulls the actin filament towards the center of the sarcomere. Although smooth muscle contractions are myogenic, the speed and strength of their contractions can be modulated by the autonomic nervous system. Postnodal nerve fibers in the parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors (mAChR) on smooth muscle cells.
These receptors are metabotropic or G protein-coupled receptors that initiate a second cascade of messengers. Conversely, the postnodal nerve fibers of the sympathetic nervous system release the neurotransmitters epinephrine and norepinephrine, which bind to adrenergic receptors that are also metabotropic. The exact effects on smooth muscle depend on the specific characteristics of the activated receptor – parasympathetic input and sympathetic entry can be excitatory (contractile) or inhibitory (relaxing). Goody, R.S. The missing link in the cycle of the transverse muscular bridge. Nature Structural Molecular Biology 10, 773–775 (2003) doi:10.1038/nsb1003-773. Which of the following statements about muscle contraction is true? One. The power stroke occurs when ATP is hydrolyzed to ADP and phosphate. b.
The power stroke occurs when ADP and phosphate dissociate from the myosin head. c. The power beat occurs when ADP and phosphate dissociate from the active center of actin. d. The power stroke occurs when Ca2+ binds the calcium head. Smooth muscles can be divided into two subgroups: one unit and several units. Smooth muscle cells from a single piece can be found in the intestines and blood vessels. Since these cells are connected to each other by lacunar junctions, they can contract as functional syncytium. Monobloc smooth muscle cells contract myogenically, which can be modulated by the autonomic nervous system. .