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Muscle and Nerve Histology
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
The plasmalemma extends deeps into the muscle fibers, forming T-tubules that carry the depolarization of action potential inside the fibers. Hence, a T-tubule with two terminal cisterns forms a triad. The triad has a voltage-gated calcium channel and ryanodine receptor. T-tubules and sarcoplasmic reticulum are essential components involved in muscle contraction.
Functional Properties of Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Excitation-contraction coupling is different in smooth muscle from that in skeletal muscle. Smooth muscle lacks T tubules, since the small cell size, the slow contraction, the lack of organization of myofibrils, and the absence of APs in many cases, do not warrant a T tubule system. Smooth muscle lacks troponin but has, instead, two other thin filament proteins, caldesmon and calponin. On stimulation, contraction is initiated by Ca2+ influx from the extracellular fluid as well as the SR, the relative contribution of these sources differs between different smooth muscle. Ca2+ influx from the SR occurs in some locations through a close association between the SR membrane and the sarcolemma, analogous to that of T tubules in skeletal muscle, as well as through second messengers (Section 6.3) that are released upon stimulation and which cause opening of Ca2+ channels in the SR membrane. The total amount of Ca2+ released by a single stimulus is usually sufficient to activate only a fraction of the cross bridges available, which allows variation in Ca2+ concentration to grade the force produced by the muscle. In the absence of an AP, Ca2+ concentration can be graded by membrane depolarization or hyperpolarization.
Striated MusclesSkeletal and Cardiac Muscles
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Within the myocyte, myofibrils are surrounded by a network of membranes, the sarcoplasmic reticulum. The sarcoplasmic reticulum in the heart is less dense and not as well developed as that in skeletal muscles. The T-tubules of the cardiac muscle are located at the Z lines, whereas they are positioned at the ends of the I-bands in skeletal muscle. Consequently, the T-tubule is linked with the terminal cisterna of the sarcoplasmic reticulum of only one sarcomere, forming a diad, rather than a triad, in the skeletal muscle. As there is less sarcoplasmic reticulum in cardiac muscle, intracellular calcium levels depend on calcium influx into the cardiac myocyte through L-type calcium channels on the sarcolemma (via activated dihydropyridine receptor), as well as its release from sarcoplasmic reticulum. The L-calcium channels open more slowly than sodium channels and remain open longer (200–300 ms). This explains why the action potential in ventricular muscle is much longer than in skeletal muscle in which the L-type calcium channels do not open. Some of this calcium causes opening of ryanodine receptors on the sarcoplasmic reticulum, and calcium diffuses out of the sarcoplasmic reticulum. All the calcium released from the sarcoplasmic reticulum, and some from the influx via the sarcolemma, binds to troponin, resulting in actin–myosin interaction and cross-bridge cycling.
The roles of human induced pluripotent stem cell-derived cardiomyocytes in drug discovery: managing in vitro safety study expectations
Published in Expert Opinion on Drug Discovery, 2020
Adult cardiomyocytes display a high length-to-width ratio, may be bi-nucleated, and form sophisticated internal structures such as T-tubules and the sarcoplasmic reticulum within the sarcomere’s Z-line. T-tubules are significant due to their role in contraction propagation [7]. Adult cardiomyocytes display Z-discs, I-, H-, A- and M- bands. In addition, adult cardiomyocytes have sarcomeres that are long (2.2 μm) and highly organized. These cells also possess large numbers of mitochondria due to the heart’s ceaseless energetic demands. Myocardial mitochondria tend to be evenly distributed throughout the cell and account for 20%-40% of cell size. In contrast, immature hiPSC-CMs tend to be round, usually mono-nucleated, and the sarcomere is disorganized and shorter (1.6 μm). Typical 2-dimensional cell constructs also do not possess T-tubules and only have disorganized Z-discs and I- bands and the sarcomeres appear to be organized but in a more isotropic fashion [8].
Gene therapy strategies for X-linked myotubular myopathy
Published in Expert Opinion on Orphan Drugs, 2018
A lot has been learned about the biology of myotubularin and XLMTM pathology; however, the mechanism by which myotubularin deficiency causes myopathy remains incompletely characterized. Studies in human tissues and animal models have described a number of alterations in XLMTM muscle that impact membrane dynamics and involve important membrane structures in muscle tissue such as the transverse-tubules (T tubule), sarcoplasmic reticulum (SR), and neuromuscular junction [15,20–22]. Other studies have revealed mitochondrial perturbations and myofiber size alterations in XLMTM patient tissues and animal models that are likely to have roles in the pathogenesis of the myopathy [2,23–25]. Ravenscroft et al. collated the key pathophysiological features that have been described in congenital myopathies, including XLMTM, and they further suggested that the perturbations underlying these pathophysiological processes represent possible targets that could be used to guide the development of therapeutic interventions [1]. Here, we examine some of the critical pathophysiological processes that have been implicated in XLMTM and, when possible, the therapeutic strategies they have spawned.
Motor activity and Becker’s muscular dystrophy: lights and shadows
Published in The Physician and Sportsmedicine, 2020
Giuseppe Lanza, Marcello Pino, Francesco Fisicaro, Carla Vagli, Mariagiovanna Cantone, Manuela Pennisi, Rita Bella, Maria Bellomo
During relaxation, the myofilaments of these sarcomeres would no longer be able to overlap and interact, so that, in the course of repeated eccentric contractions, these sarcomeres will be lengthened instantly. Eventually, this would lead to a rapid increase in tension of the adjacent sarcomeres that leads to a structural damage. If sufficient, the damage of the T-tubules together with the opening of cationic channels which are activated by mechanical stimuli, will lead to the release of intracellular calcium. The increase in sarcoplasmic calcium levels, in turn, causes the activation of proteolytic enzymes associated with destruction and subsequent repair process of the muscle fiber [12–15].