Victor Forge
Excitation-contraction coupling (ECC) is a physiological process that links the excitation of muscles by the nervous system to their mechanical contraction. ECC was first described by Galvani at the end of the 18th century, and since then, our understanding of it has increased significantly. ECC is initiated by an action potential generated by the somatic nervous system, which causes a depolarisation of the muscle fibre membrane (sarcolemma). This leads to a rapid change in the transmembrane potential, which is detected by the voltage-gated Ca2+ channel dihydropyridine receptor (DHPR) embedded in the sarcolemma. DHPR then transmits the contractile signal to another Ca2+ channel, the ryanodine receptor (RyR1), which releases a large amount of Ca2+ ions from the sarcoplasmic reticulum (SR), initiating muscle contraction.
| Characteristics | Values |
|---|---|
| Definition | The process by which muscle fiber electrical depolarization is linked to activation of muscle contraction |
| Other names | Excitation-contraction coupling (ECC) |
| Initiation | An action potential, generated by the somatic nervous system, causes a depolarization of the muscle fiber membrane (sarcolemma) |
| Action | Leads to a rapid change in the transmembrane potential, which is detected by the voltage-gated Ca2+ channel dihydropyridine receptor (DHPR) embedded in the sarcolemma |
| Role of DHPR | Transmits the contractile signal to another Ca2+ channel, ryanodine receptor (RyR1), embedded in the membrane of the sarcoplasmic reticulum (SR) |
| Role of RyR1 | Releases a large amount of Ca2+ ions from the SR that initiate muscle contraction |
| Role of Calcium | Binding of calcium to troponin causes troponin to undergo a configurational change, thereby removing tropomyosin from its blocking position on the actin filament |
| Calcium and contraction | The binding of myosin heads to actin and the subsequent release of stored energy in the myosin heads generate tension within the contractile elements |
| Calcium and relaxation | Calcium is pumped back into the sarcoplasmic reticulum by active transport, leading to muscle relaxation |
| Muscle relaxation | Occurs when the nerve impulse ceases |
| Calcium and relaxation | In the absence of calcium, tropomyosin returns to its blocking position on actin, and myosin heads are not able to bind to actin |
| Calcium and contraction | Calcium binds to calmodulin, and the Ca2+-calmodulin complex then activates the enzyme myosin light chain kinase, which phosphorylates the light chain of the contractile protein, myosin |
| Calcium and relaxation | The Ca2+-calmodulin complex activates transmembrane Ca2+ pumps to remove free Ca2+ from the cell |
| Role in skeletal muscle | Excitation-contraction coupling in skeletal muscle is the sequence of events through which the nerve fiber stimulates the skeletal muscle fiber, causing its contraction |
| Role of neuromuscular junction | The neuromuscular junction is the site where the neuronal axon terminals (synaptic terminal) of a motor neuron come in contact with the plasma membrane of the skeletal muscle fiber (motor end plate) |
| Techniques used to study ECC | CLSM combined with new techniques such as FRET (Förster resonance energy transfer) and SEER (Shifted excitation and emission ratioing) |
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What You'll Learn
ECC and calcium
Excitation-contraction coupling (ECC) is a well-organised process that transforms the electrical stimulation of the sarcolemma into muscle contraction. ECC can be categorised into three phases.
The first phase involves the initiation and propagation of an action potential along the plasma membrane. This is followed by the spread of the potential throughout the transverse tubule system (T-tubule system). In the second phase, voltage-gated calcium channels allow calcium into the cell, activating calcium release from ryanodine receptors at the sarcoplasmic reticulum, which causes contraction. The sarcoplasmic reticulum is the site of linkage between excitation and contraction.
The third phase is the cross-bridging cycle, which describes the cyclic events necessary for the generation of force or tension within the myosin heads during muscle contraction. The binding of calcium to troponin causes a configurational change, removing tropomyosin from its blocking position on the actin filament. This allows the binding of activated myosin heads with the active sites on actin, forming cross-bridges and resulting in muscle contraction.
The role of mitochondria in calcium regulation during ECC and contractile activity has been studied, but their physiological relevance for different fibre types is unclear. ECC in skeletal muscle refers to the calcium-mediated link between membrane excitation and mechanical contraction. The initiation and propagation of an action potential through the membranous system lead to the activation of calcium release units (CRU): tightly coupled dihydropyridine and ryanodine (RyR) receptors.
ECC is impaired in systolic heart failure, with a decreased influx of calcium into the cell through L-type calcium channels, resulting in reduced subsequent calcium release by the sarcoplasmic reticulum.
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ECC and muscle contraction
Excitation-contraction coupling (ECC) is a physiological process that links excitation of muscles by the nervous system to their mechanical contraction. ECC is an essential process in muscle physiology, responsible for linking electrical signals from the somatic nervous system (action potentials) to mechanical muscle contractions.
ECC is initiated with an action potential, generated by the somatic nervous system, which causes a depolarisation of the muscle fibre membrane (sarcolemma). This leads to a rapid change in the transmembrane potential, which is detected by the voltage-gated Ca2+ channel dihydropyridine receptor (DHPR) embedded in the sarcolemma.
The DHPR transmits the contractile signal to another Ca2+ channel, the ryanodine receptor (RyR1), embedded in the membrane of the sarcoplasmic reticulum (SR). This releases a large amount of Ca2+ ions from the SR, initiating muscle contraction. ECC can be categorised into three phases: the first phase involves the depolarisation and spread of an action potential along the sarcolemma and its propagation into the T tubules. The second phase involves the release of calcium from the SR and the subsequent binding of calcium to troponin molecules on the thin filament, causing a configurational change and removing tropomyosin from its blocking position on the actin filament. The third phase is the cross-bridging cycle, which describes the cyclic events necessary for the generation of force or tension within the myosin heads during muscle contraction.
ECC has been studied since the 1940s and 1950s, with major advances in understanding occurring in the last century due to improvements in electrical and optical measurements, electron microscopy, biochemistry, and molecular biology. Despite this, the molecular mechanism underpinning the communication between DHPR and RyR1 is still largely unknown.
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ECC and muscle relaxation
Excitation-contraction coupling (ECC) is a physiological process that links the excitation of muscles by the nervous system to their mechanical contraction. ECC is initiated by an action potential, generated by the somatic nervous system, which causes a depolarisation of the muscle fibre membrane (sarcolemma). This leads to a rapid change in the transmembrane potential, which is detected by the voltage-gated Ca2+ channel dihydropyridine receptor (DHPR) embedded in the sarcolemma. DHPR then transmits the contractile signal to another Ca2+ channel, the ryanodine receptor (RyR1), embedded in the membrane of the sarcoplasmic reticulum (SR). This releases a large amount of Ca2+ ions from the SR, initiating muscle contraction.
The sarcoplasmic reticulum is the site of linkage between excitation and contraction. The Ca2+ ion is associated with a certain part of the SR and is released by the influence of the electrical current field induced by depolarisation of the surface membrane. The released Ca2+ ion then activates the contractile system. The SR exerts its relaxing effect by removing the Ca2+ ion from the contractile system in vivo.
The Ca2+-calmodulin complex activates transmembrane Ca2+ pumps to remove free Ca2+ from the cell, and the ligand-receptor complex is degraded. This is followed by the removal of excess extracellular ACh by acetylcholinesterase. The final phase of muscular contraction is muscular relaxation. This occurs when the nerve impulse ceases and calcium is pumped back into the SR by active transport. In the absence of calcium, tropomyosin returns to its blocking position on actin, and myosin heads are unable to bind to actin.
In systolic heart failure, ECC can be impaired at several sites. This can cause a decrease in TN-C affinity for calcium, meaning an increase in free calcium near the troponin complex has less of an activating effect on cardiac contraction. This can lead to diastolic dysfunction.
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ECC and DHPR
Excitation-contraction coupling (ECC) is a physiological process that links excitation of muscles by the nervous system to their mechanical contraction. In skeletal muscle, ECC is initiated with an action potential, generated by the somatic nervous system, which causes a depolarisation of the muscle fibre membrane (sarcolemma). This leads to a rapid change in the transmembrane potential, which is detected by the voltage-gated Ca2+ channel dihydropyridine receptor (DHPR) embedded in the sarcolemma.
DHPRs are voltage-gated L-type Ca2+ channels, also referred to as Cav1, that are located on the T-tubule. They are composed of several subunits, including the core pore-forming and voltage-sensing α1 subunit, the transmembrane γ subunit, the extracellular α2δ subunit, and the intracellular β1a subunit. The α1 and β1a subunits have been identified as critical components in the ECC process.
DHPRs detect changes in membrane potential and transmit the contractile signal to another Ca2+ channel, the ryanodine receptor (RyR1), embedded in the membrane of the sarcoplasmic reticulum (SR). RyR1 releases a large amount of Ca2+ ions from the SR, which initiate muscle contraction. This process is known as calcium-induced calcium release (CICR).
The interaction between DHPR and RyR1 is central to the molecular mechanism of ECC in skeletal muscle. Structurally, a single RyR1 tetramer aligns opposite a tetrad of DHPR channels, suggesting a mechanical nature to their interaction. The molecular mechanism of ECC, however, is still not fully understood due to the lack of structural details. While recent studies have provided insights into the architecture of triad junctions and the intact RyR1-DHPR supercomplex, the specific mechanism of communication between DHPR and RyR1 remains largely unknown.
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ECC and RyR1
Excitation-contraction coupling (ECC) is a physiological process that links the excitation of muscles by the nervous system to their mechanical contraction. In skeletal muscle, ECC is initiated at the neuromuscular junction, where a motor neuron connects to a muscle fibre. ECC occurs at triad junctions, where dihydropyridine receptors (DHPRs) on transverse tubules sense excitation signals and then cause calcium release from the sarcoplasmic reticulum via coupling to type 1 ryanodine receptors (RyR1s), inducing the subsequent contraction of muscle filaments.
RyR1 is the largest known ion channel in mammals. It is composed of four identical subunits, each with a molecular weight of ~560 kDa. RyR1 has a pore structure similar to that of K+ channels, and it is permeable to both monovalent and divalent cations. The channel has a mushroom-like appearance, with the N-terminal domain forming 90% of the structure located in the sarcoplasmic gap between the terminal cisternae of the SR and the sarcolemma. The remaining C-terminal domain is embedded in the SR membrane and forms the channel pore.
RyR1 deficiency in congenital myopathies disrupts ECC. Mutations in RYR1, the gene encoding RyR1, are the underlying cause of various congenital myopathies, including central core disease, multiminicore disease, some forms of centronuclear myopathy, and congenital fibre-type disproportion. Patients with recessive, but not dominant, RYR1 mutations show a significant reduction in RyR protein in muscle biopsies, as well as ophthalmoplegia.
The interaction between DHPR and RyR1 is central to the molecular mechanism of ECC in skeletal muscle. DHPRs are voltage-gated L-type Ca2+ channels, also referred to as Cav1.1. The α1 and β1a subunits of DHPR have been identified as critical components in the ECC process. In contrast, the role of DHPR-β1a in transmitting the signal to RyR1 in the ECC process is still unclear. While the presence of diamond-shaped particle clusters, or "tetrads", suggests a direct mechanical interaction between RyR1 and DHPR, the interaction between them has not been observed to confirm the existence of their physical coupling.
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Frequently asked questions
Coupling in muscle refers to the process of excitation-contraction coupling (ECC), which is the sequence of events that link the sarcolemma action potential to muscle contraction and relaxation.
Excitation-contraction coupling is a physiological process that links excitation of muscles by the nervous system to their mechanical contraction. ECC is initiated by an action potential, generated by the somatic nervous system, which causes a depolarisation of the muscle fibre membrane (sarcolemma).
Calcium (Ca2+) is released from the sarcoplasmic reticulum, activating calcium release from ryanodine receptors and causing contraction. The binding of calcium to troponin causes a configurational change, removing tropomyosin from its blocking position on the actin filament. This allows for the binding of activated myosin heads with the active sites on actin, forming cross-bridges and resulting in muscle contraction.
