The transverse tubular system, or T system, consists of numerous tubular invaginations of the plasma membrane; each one is called a T tubule. T tubules penetrate to all levels of the muscle fiber and are located between adjacent terminal cisternae at the A–I junctions (see Fig. 11.8). They contain voltage-sensor proteins, depolarization-sensitive trans-membrane channels that are activated when the plasma
FIGURE 11.8 • Diagram of the organization of striated muscle fiber. This diagram illustrates the organization of the sarcoplasmic reticulum and its relationship to the myofibrils. Note that in striated muscle fibers, two transverse (T) tubules supply a sarcomere. Each T tubule is located at an A–I band junction and is formed as an invagination of the sarcolemma of striated muscle. It is associated with two terminal cisternae of the sarcoplasmic reticulum that surrounds each myofibril, one cisterna on either side of the T tubule. The triple structure as seen in cross section, where the two terminal cisternae flank a transverse tubule at the A–I band junction, is called a triad. Depolarization of the T tubule membrane initiates the release of calcium ions from the sarcoplasmic reticulum and eventually triggers muscle contraction.
membrane depolarizes. Conformational changes of these proteins directly affect gated Ca2-release channels located in the adjacent plasma membrane of the terminal cisternae. The complex of T tubule and the two adjacent terminal cisternae is called a triad.
The depolarization of the T-tubule membrane triggers the release of Ca from the terminal cisternae to initiate muscle contraction.
When a nerve impulse arrives at the neuromuscular junction, the release of neurotransmitter (acetylcholine) from the nerve ending triggers a localized plasma-membrane depolarization of the muscle cell. The depolarization, in turn, causes voltage-gated Na channels in the plasma membrane to open, allowing an influx of Na from the extracellular space into the muscle cell. The influx of Na results in general depolarization, which spreads rapidly over the entire plasma membrane of the muscle fiber. When the depolarization encounters the opening of the T tubule, it is transmitted along the membranes of the T system into the depths of the cell. Electrical charges activate voltage-sensor proteins located in the membrane of the T tubule. These proteins have the structural and functional properties of Ca2 channels. During skeletal muscle depolarization, short activation of these sensors is not sufficient to open Ca2 channels. Thus, Ca2 transport from the lumen of the T tubule into the sarcoplasm does not occur and is not essential to trigger the contraction cycle. Instead, activation of these sensors opens gated Ca2-release channels in adjacent terminal sacs of the sarcoplasmic reticulum, causing the rapid release of Ca2 into the sarcoplasm. The increased concentration of Ca2 in the sarcoplasm initiates contraction of the myofibril by binding to the TnC portion of the troponin complex on the thin filaments (see page 316). The change in molecular conformation of TnC causes the TnI to dissociate from the actin molecules, allowing the troponin complex to uncover myosin-binding sites on the actin molecules. The myosin heads are now free to interact with actin molecules to initiate the muscle contraction cycle.
Simultaneously, a Ca2-activated ATPase pump in the membrane of the sarcoplasmic reticulum transports Ca2 back into the terminal cisternae. The resting concentration of Ca2 is restored in the cytosol in less than 30 milliseconds. This restoration of resting Ca2 concentration near the myo filaments normally causes contraction to stop. Contraction will continue, however, as long as nerve impulses continue to depolarize the plasma membrane of the T tubules.