T-tubule system

Muscle contraction is initiated by a signal from a motor nerve. This triggers an action potential, which is propagated along the muscle plasma membrane to the T-tubule system and the sarcotubular reticulum, where a sudden large electrically excited release of Ca " into the cytosol occurs. Accessory proteins closely associated with actin (troponins T, I, and C) together with tropomyosin mediate the Ca -dependent motor command within the sarcomere. Other accessory proteins (titin, nebulin, myomesin, etc.) serve to provide the myofibril with both stability... 

In the sarcoplasm of resting muscle, the concentration of Ca + is 10 to 10 mol/L. The resting state is achieved because Ca + is pumped into the sarcoplasmic reticulum through the action of an active transport system, called the Ca + ATPase (Figure 49-8), initiating relaxation. The sarcoplasmic reticulum is a network of fine membranous sacs. Inside the sarcoplasmic reticulum, Ca + is bound to a specific Ca -binding protein designated calsequestrin. The sarcomere is surrounded by an excitable membrane (the T tubule system) composed of transverse (T) channels closely associated with the sarcoplasmic reticulum. 

When the sarcolemma is excited by a nerve impulse, the signal is transmitted into the T tubule system and a release channel in the nearby sarcoplasmic reticulum opens, releasing Ca + from the sarcoplasmic reticulum into the sarcoplasm. The concentration of Ca in the sarcoplasm rises rapidly to 10 mol/L. The Ca -binding sites on TpC in the thin filament are quickly occupied by Ca +. The TpC-4Ca + interacts with Tpl and TpT to alter their interaction with tropomyosin. Accordingly, tropomyosin moves out of the way or alters the conformation of F-actin so that the myosin head-ADP-P (Figure 49-6) can interact with F-actin to start the contraction cycle. 

Ca ion concentration As an action potential travels along the muscle fibre and into the interior of the fibre, via the T-tubule system, ions are released from the sarcoplasmic reticulum (Chapter 13). This increases the concentration of Ca + ions in the cytosol which is followed by an increase in concentration within the mitochondria. 

Figure 13.13 A diagrammatic three-dimensional view of part of a single muscle fibre showing the T-tubule system and the sarcoplasmic reticulum. The T-tubules are located within the fibre and are attached to the reticulum. This is a sheet of anastomosing flattened vesicles that surround each myofibril like a net stocking.

At the ultrastructural level, flatworm muscle resembles smooth muscle with individual, non-striated myofibrils being delimited by the sarcolemma and interconnected by gap junctions. Also, flatworm muscles lack a T-tubule system that is characteristic of striated muscle in other animal groups. The contractile portion of flatworm myofibrils contains thick myosin and thin actin filaments that connect with the sarcolemma via attachment plaques or desmo-somes. Actomyosin cross-bridges have been reported and where overlap has been observed, ratios that vary from 9 1 to 12 1 have been observed. Although flatworm muscle is mostly non-striated, pseudo-striated (e.g. in the tail of schistosome cercariae Dorsey et al., 2002 Mair et al., 2003) and obliquely striated (e.g. tentacular bulb of the trypanorhynch, Crillotia eri-naceus Ward et al., 1986) muscles have been reported. It is presumed that the role played by these structures has demanded the development... 

Non-clathrin-coated pit internalization can occur through smooth imagination of 150-300 nm vesicles or via potocytosis. This pathway has been shown to be involved in the transport of folate and other small molecules into the cytoplasm. Plasmids are taken up by muscles through the T-tubules system and caveolae via potocytosis. Muscle cells appear to take up plasmids through the T-tubule system and caveolae via potocytosis. Apart from coated or uncoated pit pathways, cells may also take up plasmid/cationic carrier complexes via plasma membrane destabilization. Particles greater than 200 nm in diameter are not... 

Rhabdomyoma in man (T-tubule system in skeletal muscle) Lattice-like paractystalls D [160]... 

Cubic membranes have also been foimd in Aves. The study by Ishikawa [18] on the development of the transverse tubule membrane (T-tubule) system in cultured skeletal muscle cells derived from chick embryo represents one of the more arresting examples of cubic membranes that are produced as invaginations of the PM. Indeed, Ishikawa s model for the T-tubule is in many respects similar to that of cubic membranes. Although there were no comments in the original report [18] regarding the symmetry of the "tubular network", the model is in many respects similar to the D-surface. 

Fig. 47.3. Events leading to sarcoplasmic reticulum calcium release in skeletal muscle. 1. Acetylcholine, released at the synaptic cleft, binds to acetylcholine receptors on the sar-colemma, leading to a change of conformation of the receptors such that they now act as an ion pore. This allows sodium to enter the cell and potassium to leave. 2. The membrane polarization that results from these ion movements is transmitted throughout the muscle fiber by the T-tubule system. 3. A receptor in the T-tubules (the dihydropyridine receptor, DHPR) is activated by membrane polarization (a voltage-gated activation) such that activated DHPR physically binds to and activates the ryanodine receptor in the sarcoplasmic reticulum (depolarization-induced calcium release). 4. The activation of the ryanodine receptor, which is a calcium channel, leads to calcium release from the SR into the sarcoplasm. In cardiac muscle, activation of DHPR leads to calcium release from the T-tubules, and this small calcium release is responsible for the activation of the cardiac ryanodine receptor (calcium-induced calcium release) to release large amounts of calcium into the sarcoplasm.

Modeling Activation Dynamics. As noted is Sec. 6.5.1 ( Neural Excitation of Muscle ), muscle cannot activate or relax instantaneously. The delay between excitation and activation (or the development of muscle force) is due mainly to the time taken for calcium pumped out of the sarcoplasmic reticulum to travel down the T-tubule system and bind to troponin (Ebashi and Endo, 1968). This delay is often modeled as a first-order process (Zajac and Gordon 1989 Pandy et al., 1992) ... 

In the zone of Z membrane, invaginations of sarcolemma regularly occur, constituting the secondary system of T tubules or transversal, which is not connected to the sarcoplasmic reticulum. Functionally, these ones intervene by a trap system in the caption of Ca ions released during the muscle excitation and in metabolic exchanges of the fibrillar apparatus T tubules system conveys the excitation from the sarcolemma to the fibrillar apparatus, causing the fibres contraction, by releasing Ca. ... 

Figure 10). To consider the source of this unexplained heat, it must be recalled that contraction is initiated by the depolarisation of the sarcolemma spreading to the T-tubule system. This causes the Ca bound to calsequestrin in the sarcoplasmic reticulum to be released into the sarcoplasm (cytosol) and bind to troponin C [4]. It is the entropy change caused by the movement of the Ca ions that accounts for at least some of the unexplained heat. Another source of it that is difficult to quantify accurately is the splitting of ATP in the pumping of Ca ions back to the sarcoplasmic reticulum to mark the end of the contraction cycle. The exact stoichiometry of this relationship is not known but it is maximally 2 ATP per Ca ion.

According to Schneider and Chandler (1973), depolarization of the T-tubules affects sensors which open Ca " channels in the SR. The sensors are modified Ca channels which act as voltage sensors (Tanabe et al., 1987). The signal from the sensor reaches the SR and opens the Ca channels with the release of Ca to the myoplasm. The Ca channels in the SR system are opened by micromolar [Ca ], mM [ATP], and caffeine but are inhibited by Mg (Smith et al., 1986 Rosseau et al., 1988). The channels are closed in resting muscle and are opened when the voltage sensor is activated. 

Using the reconstitution approaches described above, we have demonstrated that phosphorylation of the skeletal muscle Ca channels by PKC results in activation of the channels [108], In the fluo 3-containing liposomes, channels phosphorylated by PKC exhibited a two-fold increase in the rate and extent of Ca " influx [108], Using the lipid bilayer-T-tubule membrane reconstitution system we are currently analyzing the effects of PKC-catalyzed phosphorylation at the single channel level [133], The demonstration that these channels undergo phosphorylation as a result of activation of PKC in intact skeletal muscle cells has not yet been achieved. 

T-system membrane results in an interaction between the T-tubules and the SR at specialised junctions, known as excitation-contraction coupling units. Here the two membranes are finked by a foot process consisting of two Ca ion channels that function in concert. 

As in skeletal muscle, the action potential is transmitted into the cardiomyocytes by a T-system. The depolarisation opens Ca ion channels in the T-system (i.e. the plasma membrane) which leads to a small increase in the cytosolic ion concentration. This activates Csl ion channels in the sarcoplasmic reticulum (a process known as a Ca -induced Ca ion release) which results in the movement of more Ca ions into the cytosol. The amount of Ca ion released from the reticulum varies according to the stimulation of the ion channel, i.e. the amount of Ca ions released from the T-tubule. This provides for variations in the cytosolic Ca ion concentration and hence in the force of contraction. 

A closer look at striated muscle fibers shows that they themselves are assemblies of fine, hairlike structures known as myofibrils (Fig. 1A, B). Myofibrils may be about 2 to 5 jxm in diameter, with cell organelles such as mitochondria and membranous systems called T-tubules and the sarcoplasmic reticulum (SR) sandwiched between them (Fig. 2B). 

Furukawa, T., Ono, Y., and Tsuchiya, H. (2001). Specific interaction of the potassium channel beta-subunit minKwith the sarcomeric protein T-cap suggests a T-tubule-myofibril linking system. J. Mol. Biol. 313, 775-784. 

Expression of Ion Channels and Pumps Differences in the expression of voltage-gated ion channels at the sarco-lemma, T-tubular system, or SR may determine the excitation of a muscle fiber in response to neurotransmitter release. A decrease in the amount of T-tubules measured per unit volume or voltage-gated Na channels would potentially act to decrease the amplitude of the muscle action potential. Similarly, Ca entry and release from intracellular stores (mainly the SR) influence thin filament activation and, ultimately, force generation. 

Sarcoplasm - contains multiple nuclei, located peripherally beneath sarcolemma, sarcoplasmic reticulum, mithocondria, which are specialised into an intense oxidative mechanism, working into a medium rich in hemoglobin that fixes the oxygen. All these peculiarities just reflect the specialisation of muscle fiber with a view to perform the contractile function. Sarcoplasmic reticulum and T tubules is a membranous system of longitudinal tubules, in the zone of H band, and terminal cisterns (flattened reservoirs for Ca ) that forms closely meshed network around each myofibril. 

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