Muscle contraction is turned on when sufficient amounts of Ca2+ bind to troponin. This occurs when the Ca2+ concentration of the sarcoplasm rises above 10-6 molar. In order for muscle relaxation to occur, therefore, the Ca2+ concentration of the sar-coplasm must be lowered to below this level. Muscle relaxation is produced by the active transport of Ca2+ out of the sarcoplasm into the sarcoplasmic reticulum (fig. 12.15). The sarcoplasmic reticulum is a modified endoplasmic reticulum, consisting of interconnected sacs and tubes that surround each myofibril within the muscle cell.
Most of the Ca2+ in a relaxed muscle fiber is stored within expanded portions of the sarcoplasmic reticulum known as terminal cisternae. When a muscle fiber is stimulated to contract by either a motor neuron in vivo or electric shocks in vitro, the stored Ca2+ is released from the sarcoplasmic reticulum by passive diffusion through membrane channels termed calcium release channels (fig. 12.16), so that the Ca2+ can attach to troponin. When a muscle fiber is no longer stimulated, the Ca2+ is actively transported back into the sarcoplasmic reticulum. Now, in order to understand how the release and uptake of Ca2+ is regulated, one more organelle within the muscle fiber must be described.
The terminal cisternae of the sarcoplasmic reticulum are separated only by a very narrow gap from transverse tubules (or T tubules). These are narrow membranous "tunnels" formed from and continuous with the sarcolemma (muscle plasma membrane). The transverse tubules thus open to the extracellular environment through pores in the cell surface and are able to conduct action potentials. The stage is now set to explain exactly how a motor neuron stimulates a muscle fiber to contract.
The release of acetylcholine from axon terminals at the neu-romuscular junctions (motor end plates), as previously described, causes electrical activation of skeletal muscle fibers. End-plate potentials (analogous to EPSPs—chapter 7) are produced that generate action potentials. Action potentials in muscle cells, like those in nerve cells, are all-or-none events that are regenerated along the plasma membrane. It must be remembered that action potentials involve the flow of ions between the extracellular and intracellular environments across a plasma membrane that separates these two compartments. In muscle cells, therefore, action potentials can be conducted into the interior of the fiber across the membrane of the transverse tubules.
■ Figure 12.14 The role of Ca2+ in muscle contraction. The attachment of Ca2+ to troponin causes movement of the troponin-tropomyosin complex, which exposes binding sites on the actin. The myosin cross bridges can then attach to actin and undergo a power stroke.
Action potentials in the transverse tubules cause the release of Ca2+ from the sarcoplasmic reticulum. This process is known as excitation-contraction coupling (table 12.3). Since the transverse tubules are not physically continuous with the sar-coplasmic reticulum, however, there must be some mechanism to permit communication between these two organelles. It is currently believed that there may be a direct coupling, on a molecular level, between voltage-regulated Ca2+ channels in the transverse tubules and the Ca2+ release channels in the sarcoplasmic reticulum. The Ca2+ release channel proteins of the sarcoplasmic reticulum have a part that extends into the cytoplasm. This part, which has a footlike appearance in the electron microscope, may be able to interact directly with the Ca2+ channel proteins of the transverse tubules (fig 12.16).
This arrangement has been described as an electromechanical release mechanism, because changes in membrane voltage
Transverse tubule Sarcoplasmic reticulum
■ Figure 12.15 The sarcoplasmic reticulum. This figure depicts the relationship between myofibrils, the transverse tubules, and the sarcoplasmic reticulum. The sarcoplasmic reticulum (green) stores Ca2+ and is stimulated to release it by action potentials arriving in the transverse tubules.
(action potentials) in the transverse tubules cause a change in protein conformation of calcium channels, which are mechanically linked to other calcium channels in the sarcoplasmic retic-ulum. There is also evidence that the Ca2+ flow through the channels in the transverse tubules may stimulate the opening of other calcium channels in the sarcoplasmic reticulum. This is termed a Ca2+-induced Ca2+ release mechanism, and has been shown to be the major mechanism for excitation-contraction coupling in heart muscle. By these mechanisms, Ca2+ can be released from the sarcoplasmic reticulum, bind to troponin, and stimulate muscle contraction.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.