What is the sarcolemma in muscle?
The sarcolemma ( sarco (from sarx) from Greek; flesh, and lemma from Greek; sheath) also called the myolemma, is the cell membrane of a muscle cell. It consists of a lipid bilayer and a thin outer coat of polysaccharide material ...
What is the name of the muscle cell that invaginates into the sarcoplasm?
A special feature of the sarcolemma is that it invaginates into the sarcoplasm of the muscle cell, forming membranous tubules radially and longitudinally within the fiber called T-tubules or transverse tubules.
What is the sarcolemma?
The sarcolemma ( sarco (from sarx) from Greek; flesh, and lemma from Greek; sheath) also called the myolemma, is the cell membrane of a muscle cell. It consists of a lipid bilayer and a thin outer coat of polysaccharide material ( glycocalyx) that contacts the basement membrane. The basement membrane contains numerous thin ...
What is the basement membrane?
The basement membrane contains numerous thin collagen fibrils and specialized proteins such as laminin that provide a scaffold to which the muscle fiber can adhere. Through transmembrane proteins in the plasma membrane, the actin skeleton inside the cell is connected to the basement membrane and the cell's exterior.
Why is the lipid nature of the membrane important?
The lipid nature of the membrane allows it to separate the fluids of the intra- and extracellular compartments, since it is only selectively permeable to water through aquaporin channels. As in other cells, this allows for the compositions of the compartments to be controlled by selective transport through the membrane.
Which layer of the muscle fiber fuses with the tendon fiber?
At each end of the muscle fiber, the surface layer of the sarcolemma fuses with a tendon fiber, and the tendon fibers, in turn, collect into bundles to form the muscle tendons that adhere to bones. The sarcolemma generally maintains the same function in muscle cells as the plasma membrane does in other eukaryote cells.
How does calcium transient work?
The calcium transient is initiated in response to sarcolemmal depolarization by extracellular calcium (Ca2+) influx through voltage-dependent L-type Ca2+channels ; this calcium influx brings about the release of stored Ca2+from the sarcoplasmic reticulum (SR), via Ca2+release channels (ryanodine receptor 2, RyR2). This latter step, known as calcium-induced calcium release, amplifies the amount of calcium available for myofilament binding and the force for generating actin–myosin cross-bridges. Relaxation results from closure of the release channels, resequestration of Ca2+by the energy-dependent sarcoplasmic-endoplasmic reticulum calcium ATPase (SERCA2), and cross-bridge dissolution. To maintain steady-state calcium homeostasis, the amount of Ca2+entering the cell with each contraction must be removed before the subsequent contraction. To this end, the NCX acting in the forwardmode (Na+in, Ca2+out) competes with SERCA2 for Ca2+and pumps [Ca2+]iinto the extracellular space.
What is the sarcoplasmic reticulum?
The sarcoplasmic reticulum forms a fine plexus around the myofibrils. Excitation of the sarcolemma and T tubules causes Ca2+ release from the sarcoplasmic reticulum and initiation of contraction by the myofilaments. Several important proteins are localized to the triads.
What is the site where calcium enters and leaves the cell?
The sarcolemma or cell membrane is the site where calcium enters and leaves the cell through a distribution of ion channels, transporters, and pumps. The T-tubules are invaginations of the sarcolemma that form a permeability barrier between the cytosol and the extracellular space ( Brette and Orchard, 2003 ).
What is the negative potential of a sarcolemma?
The negative potential is derived from the disequilibrium of ionic concentrations (mostly Na+ and K +) across the membrane and is generated partly by the action of the Na + /K + ATPase pump, which extrudes three Na + ions for every two K + ions taken up. This results in the cytoplasm having a much higher K + concentration but much lower Na + concentration than the extracellular fluid. The remainder of the membrane potential is derived from the tendency of ions to diffuse down their electrochemical gradients across the semipermeable membrane.
What is the role of gCl in sarcolemma?
1). The main physiological role for the large gCl is to maintain the electrical stability of the sarcolemma. In fact in pioneering studies, Bryant showed that the hyperexcitability recorded in the intercostal muscle of myotonic “fainting” goat was related to an abnormally low gCl, and could be reproduced by 9-AC, putting the basis for the discovery of a large series of genetic diseases due to mutations in membrane ion channels (Bryant and Morales-Aguilera, 1971).
What are the features of muscle fibers?
Other features seen on ultrastructural examination of muscle fibers are nuclei and the sarcoplasm and its organelles. A typical muscle fiber has thousands of nuclei located beneath the sarcolemma throughout the length of the fiber. The sarcoplasm contains many of the elements found in the cytoplasm of other tissues.
What is the T-tubule system?
T-tubules are invaginations of the sarcolemma, extending into the interior of the muscle fiber as the sarcotubular system. Depolarization of the sarcolemma is propagated throughout the interior of the muscle fiber through this system.
What is the reversible binding of ACh with AChRs?
Excitation of the myofiber is initiated by the reversible binding of ACh with AChRs. The binding of ACh with AChR (two ACh molecules/receptor) results in a local depolarization of the postsynaptic membrane caused by the transient-increased conductance of the AChR cation ion channels to sodium and potassium ions. The amplitude of the end-plate potential (depolarization) is proportional to the number of ACh-AChR complexes formed. At rest, individual quanta of ACh are spontaneously released at a slow rate and cause transient, low-amplitude depolarizations at the end plate. These are referred to as miniature end-plate potentials (MEEPs). The interior of a resting muscle fiber has a resting potential of about −95 mV.The binding of ACh to AChRs is transient, and its effects are abolished by diffusion of ACh away from the receptors and its hydrolysis by AChE. With the arrival of a nerve action potential, approximately 200 quanta of ACh are released, and with the increased number of ACh-AChR combinations, there is a greater conductance of sodium and potassium ions that form a large amplitude depolarization, the end-plate potential (EEP). When the amplitude of the EEP exceeds threshold (approximately −50 mV), a wave of depolarization (muscle action potential, MAP) is generated over the sarcolemma, away from the end plate in all directions. The MAP is propagated by voltage-gated sodium channels over the surface of the myofiber and into its depths via transverse (T) tubules. The T tubules are invaginations of the sarcolemma that tranverse the long axis of the myofiber, and their lumina openly communicate with the extracellular fluid space ( Engel, 2004 ).
What is the role of gCl in sarcolemma?
1 ). The main physiological role for the large gCl is to maintain the electrical stability of the sarcolemma. In fact in pioneering studies, Bryant showed that the hyperexcitability recorded in the intercostal muscle of myotonic “fainting” goat was related to an abnormally low gCl, and could be reproduced by 9-AC, putting the basis for the discovery of a large series of genetic diseases due to mutations in membrane ion channels ( Bryant and Morales-Aguilera, 1971 ).
How does myofiber contract?
Figure 15-1. Excitation of myofibers to contract involves neuromuscular transmission and the subsequent release of calcium ions into the sarcoplasm. Arrival of an impulse at the axon terminal activates voltage-gated calcium ion channels, resulting in the influx of calcium ions that initiate the calcium-dependent release of the neurotransmitter acetylcholine (ACh) by exocytosis. Liberated ACh diffuses across the synaptic cleft to bind with ACh receptors (two molecules of ACh per receptor) on the postsynaptic sarcolemma. Binding of ACh with AChRs increases the conductance of sodium and potassium ions across the postsynaptic membrane to produce a local end-plate potential at the neuromuscular junction. The end-plate potential generates a muscle action potential that spreads away from the neuromuscular junction in all directions over the surface of the myofiber and into its depths via the transverse (T) tubules. Within the depths of the myofibers, excitation is coupled to contraction through the release of calcium ions from terminal cisternae of the sarcoplasmic reticulum (SR) through calcium release channels of the terminal cisternae. The calcium release channels form small “feet” that extend from the terminal cisternae to the T tubules. The liberated calcium ions bind to the regulatory protein troponin and release the inhibitory action of the regulatory proteins on the contractile events that lead to sliding of the thin (actin) and thick (myosin) filaments. The liberated ACh is subsequently hydrolyzed by AChE (acetylcholinesterase) within the basal lamina of the synaptic cleft.
What happens when the sarcolemma is depolarized?
Depolarization of the sarcolemma leads to opening of voltage-gated Ca2+ channels and influx of Ca 2+ from the extracellular space. This Ca 2+ pulse can also trigger the release of intracellular Ca 2+ from the sarcoplasmic reticulum (Ca 2+ -induced Ca 2+ release, CICR). Contraction is then triggered by elevated intracellular Ca 2+ levels.
What causes fatigue in myotonia congenita?
Impairment of sarcolemma excitability due to K+ -mediated depolarization of the contracting fibers may result in excessive fatigue in myotonia congenita (MC), type 1 myotonic dystrophy (MD), hyperkalemic familial periodic paralysis (HKFPP), and paramyotonia congenita. In hereditary myotonic disorders (MC and MD), the fatigue appears within seconds of voluntary or stimulated contractions, but the paresis gradually wears off (warm-up phenomenon) as the exercise continues. The abnormal genotype expression of Cl – channel in MC and possible abnormality of Na + channel in MD result in impairment of excitability of sarcolemma. However, in MD patients, in addition to impairment of sarcolemma, both mitochondrial and glycogenolytic functions are affected and may contribute to fatigue and weakness. In HKFPP and paramyotonia congenita (with genetic abnormality of Na + channels), fatigue occurs less rapidly (in minutes) and tends to become worse after the voluntary contractions cease than in myotonic disorders (seconds).
What is the site where calcium enters and leaves the cell?
Sarcolemma . The sarcolemma or cell membrane is the site where calcium enters and leaves the cell through a distribution of ion channels, transporters, and pumps. The T-tubules are invaginations of the sarcolemma that form a permeability barrier between the cytosol and the extracellular space ( Brette and Orchard, 2003 ).
What is the role of the sarcolemma in muscle contraction?
The sarcolemma maintains the intracellular milieu, actively transports substrates into the muscle cell, serves as a docking location for proteins originating in the basement membrane and cytoskeleton, and also transmits neural excitatory impulses that lead to muscle contraction. Facilitated diffusion of glucose across the sarcolemma occurs via glucose transporters (GLUT). GLUT-1 is constitutively present in the sarcolemma and provides basal amounts of glucose uptake, whereas GLUT-4 is present in the endosomes in the sarcoplasma, which migrate to and then dock and fuse with the sarcolemma when stimulated by insulin and contraction-dependent processes. Long-chain fats are transported across the sarcolemma by fatty acid translocase.
What receptors are involved in CK elevation?
The presence of 5-HT2A receptor in skeletal muscle and the 5HT2A receptor blockade caused by the atypicals could produce this CK elevation through a sarcolemmapermeability enhancing effect.
What are the findings of histopathological investigation showing muscle damage?
Histopathological Investigation Showing Muscle Damage The findings including the separations between the myofibrils, increased connective tissue between the muscle fibers, loss of striations and the circular formation of the nuclei that were transferred to the centrum beneath the sarcolemmawere highest in the groups that were sacrificed one day after the exhausting exercise, both in the T group and UT group (Figure 3).
What is the mechanism of muscle contraction?
Muscle contraction occurs when the summation of acetylcholine receptor activation reaches the threshold to trigger voltage dependent sodium channel activation in the sarcolemmaoutside the neuromuscular junction and subsequent action potential generation and depolarization of the muscle fiber.
What is Fig. 274?
Fig. 274 Saturated vapour pressure. The effect of ambient temperature on the vapour pressure at the surface of a mesophyll.
What is the membrane of a muscle fiber?
The plasma membrane of a muscle fiber; formerly, the delicate connective tissue of the endomysium was included under this term by some.
Why is Desmin important?
Desmin is important to the ultrastructure of muscle as it is a constituent of costameres and intermediate filaments that anchor myofibrils sarcolemmaand link adjacent myofibrils to each other at the Z-disk level, respective ly.
What are the hypotheses for cocaine vasospasm?
Hypotheses include cocaine-induced vasospasm with resultant muscle ischemia, excessive energy demands placed on the sarcolemma, and direct toxic effects on myocytes.
What is the name of the membrane in the muscle?
Sarcolemma is a form of membrane in a muscle in the human body.
Which sheath incloses a striated muscular fiber?
the very thin transparent and apparently homogeneous sheath which incloses a striated muscular fiber; the myolemma
