The mechanism of electromechanical coupling, sliding theory. Electromechanical coupling in muscles

Electromechanical interface is a cycle of sequential processes that begins with the occurrence of an action potential on the sarcolemma and ends with the contractile response of the muscle.

The generally accepted model of muscle contraction is the sliding filament model, according to which the contractile process occurs as follows.

Under the influence of a nerve impulse, sodium channels open in the sarcolemma, and Na + ions enter the muscle cell, causing excitation (depolarization) of the sarcolemma.

Electrochemically, the excitation process is transmitted to the sarcoplasmic reticulum. As a result, the permeability of this membrane structure for Ca++ ions increases and they are released into the cytoplasmic fluid (sarcoplasm) filling the muscle fiber. An increase in Ca ++ concentration from 10 –7 to 10 –5 mol/l stimulates the cyclic work of myosin “bridges”. The “bridge” binds to actin and pulls it towards the center A-zone, to the area where the myosin filaments are located, moving to a distance of 10–12 nm. Then it splits off from actin, binds to it at another point and again pulls it into the right side. The continuous movement of actin filaments occurs as a result of the alternating work of “bridges”. The frequency of their movement cycles appears to be regulated depending on the load on the muscle and can reach 1000 Hz. “Bridges” have ATPase activity, stimulate the breakdown of ATP and use the energy released during this process for their work.

The return of the muscle to its original state is due to the reverse transitions of Ca ++ ions from the sarcoplasm to the reticulum due to the work of calcium pumps and the fact that K + passively leaves the muscle cell, causing repolarization of the sarcoplema.

The mechanical force developed by a muscle during contraction depends on the size of its cross-section, the initial length of the fibers and a number of other factors. The muscle force per 1 cm 2 of its cross section is called absolute muscle strength. For humans, it varies between 50–100. The strength of the same human muscles depends on a number of physiological conditions: age, gender, training, etc. It should also be noted. That in different muscle cells of the body the process of conjugation occurs somewhat differently. For example, the delay in the onset of contraction relative to the onset of excitation of the sarcolemma in skeletal muscles ax is 20 ms, in the heart it is slightly more (up to 100 ms).

* If a molecule or part of a molecule has a non-zero dipole moment or electric charge, then they are called polar

Transmission of the command to contract from the excited cell membrane to the myofibrils deep in the cell (electromechanical coupling) includes several sequential processes in which Ca2+ ions play a key role.

In the resting state, thread sliding in the myofibril does not occur, since the binding centers on the actin surface are closed by tropomyosin protein molecules (Fig. 7.3, A, B). Excitation (depolarization) of the myofibril and muscle contraction itself are associated with the process of electromechanical coupling, which includes a series of sequential events.

As a result of the activation of the neuromuscular synapse on the postsynaptic membrane, an EPSP arises, which generates the development of an action potential in the area surrounding the postsynaptic membrane.

Excitation (action potential) spreads along the myofibril membrane and, through a system of transverse tubules, reaches the sarcoplasmic reticulum. Depolarization of the sarcoplasmic reticulum membrane leads to the opening of Ca2+ channels in it, through which Ca2+ ions enter the sarcoplasm (Fig. 7.3, B).

Ca2+ ions bind to the protein troponin. Troponin changes its conformation and displaces the tropomyosin protein molecules that covered the actin binding centers (Fig. 7.3, D).

Myosin heads attach to the opened binding centers, and the contraction process begins (Fig. 7.3, E).

Rice. 7.3. Mechanism of coupling of excitation and contraction:

1 – transverse tubule of the sarcoplasmic membrane, 2 – sarcoplasmic reticulum, 3 – Ca2+ ion, 4 – troponin molecule, 5 – tropomyosin molecule. Explanation - in the text

The development of these processes requires a certain period of time (10–20 ms). The time from the moment of excitation of the muscle fiber (muscle) to the beginning of its contraction is called the latent period of contraction.

We can distinguish the main 4 di. Electromechanical pairing V cage skeletal muscles cells (electromechanical pairing)...

Electromechanical pairing V cage skeletal muscles. Transmission of the command to contract from the excited cell membrane to the myofibrils in depth cells(uh...more details."

Electromechanical pairing V cage skeletal muscles. Transmission of the command to contract from the excited cell membrane to the myofibrils deep in the cell. Loading.

Mechanical model muscles Hilla. Skeletal muscle at rest, its mechanical behavior is a viscoelastic material. In particular, it is characterized by stress relaxation.

Physiological properties of atypical myocardium: 1) excitability is lower than that of skeletal muscles, but higher than that cells contractile myocardium, so this is where the generation of nerve impulses occurs

Structure muscular cells And muscular proteins. Basic structural unit skeletal muscular fabric is muscular fiber consisting of...
When the heart contracts muscles(systole) blood is ejected from the heart into the aorta and the arteries branching from it.

Physical and physiological properties skeletal, hearty and smooth muscles. Based on morphological characteristics, three groups are distinguished muscles: 1) striated muscles (skeletal muscles)

2) control apparatus - a group of nervous cells, in which a model of the future result is formed; 3) reverse afferentation - secondary afferent nerve impulses that go to the acceptor of the result of the action to evaluate the final result

Based on morphological characteristics, three groups are distinguished muscles: 1) striated muscles (skeletal muscles... more details".
Myoneural (nervous) muscular) synapse – formed by the axon of a motor neuron and muscular cell.

Manifested by widespread glycogen deposition in the liver, kidneys, heart muscle, in area nervous system, skeletal muscles.
5) determination of glycogen in liver biopsy, V cells peripheral blood

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Electromechanical coupling is a cycle of sequential processes that begins with the occurrence of an AP action potential on the sarcolemma (cell membrane) and ends with the contractile response of the muscle.

Violation of the sequence of pairing processes can lead to pathologies and even death. The main stages of this process can be traced according to the diagram in Fig. 7.11.

Rice. 7.11. Scheme of electromechanical coupling in a cardiomyocyte (M - cell membrane-sarcolemma, SR - sarcoplasmic reticulum, MF ...
- myofibril, Z - z-discs, T - T-system of transverse tubules); 1 - entry of Na + and 2 - entry of Ca 2+ into the cell upon excitation of the membrane, 3 - "calcium volley", 4 - active transport of Ca 2+ into the SR, 5 - release of K + from the cell, causing repolarization of the membrane, 6 - active transport of Ca 2+ from the cell

The process of cardiomyocyte contraction occurs as follows

1 - when a stimulating pulse is applied to the cell, fast (activation time 2 ms) sodium channels open; Na+ ions enter the cell, causing depolarization of the membrane

2 - as a result of depolarization of the plasma membrane, voltage-dependent openings open in it and in T-tubules; slow calcium channels (lifetime 200 ms), and Ca 2+ ions come from the extracellular environment, where their concentration is ≈ 2 10 -3 mol / l, into the cell (intracellular concentration of Ca 2+ ≈ 10 -7 mol / l);

3 - calcium entering the cell activates the membrane of the SR, which is an intracellular depot of Ca 2+ ions (in the SR their concentration reaches ≈ 10 -3 mol / l), and releases calcium from the vesicles of the SR, resulting in the so-called “calcium volley” ". Ca 2+ ions from the SR enter the actin-myosin complex of the MF, open the active centers of the actin chains, causing the closure of the bridges and the further development of strength and shortening of the sarcomere;

4 - at the end of the process of myofibril contraction, Ca 2+ ions, with the help of calcium pumps located in the SR membrane, actively end up inside the sarcoplasmic reticulum;

5 — the electromechanical coupling process ends with K+ passively leaving the cell, causing membrane repolarization;

6 - Ca 2+ ions are actively released into the extracellular environment using calcium pumps of the sarcolemma

Thus, in the cardiomyocyte, electromechanical coupling occurs in two stages: first, a small incoming flow of calcium activates the SR membranes, promoting a greater release of calcium from the intracellular store, and then, as a result of this release, the sarcomere contracts. The two-step conjugation process described above has been proven experimentally. Experiments have shown that: a) the absence of calcium flow from outside the cell j Ca stops the contraction of sarcomeres, b) under conditions of a constant amount of calcium released from the SR, a change in the amplitude of the calcium flow leads to a well-correlated change in the force of contraction. The flow of Ca 2+ ions into the cell thus performs two functions: it forms a long (200 ms) plateau of the action potential of the cardiomyocyte and participates in the process of electromechanical coupling.

It should be noted that not in all muscle cells of the body the process of conjugation occurs, as in a cardiomyocyte. Thus, in the skeletal muscles of warm-blooded animals the action potential is short (2-3 ms) and there is no slow flow of calcium ions in them. In these cells, the T-system of transverse tubules is highly developed, approaching directly to the sarcomeres close to the z-discs. Changes in membrane potential during depolarization are transmitted through the T-system directly to the SR membrane in such cells, causing a burst release of Ca 2+ ions and further activation of contraction (3, 4, 5).

Common to all muscle cells is the process of releasing Ca 2+ ions from intracellular stores - the sarcoplasmic reticulum and further activation of contraction. The course of calcium release from the SR is experimentally observed using the protein aequorin, which luminescent in the presence of Ca 2+ ions, which was isolated from luminous jellyfish.

The delay in the onset of contraction development in skeletal muscles is 20 ms, and in cardiac muscles it is slightly longer (up to 100 ms).

The curare poison, which is used by Amazon hunters, paralyzes the victim precisely due to the fact that the molecules of this poison, once in the blood, penetrate the acetylcholine receptors and settle on them, so that when acetylcholine itself comes to these receptors, there are no more free places, and the transfer process the signal for muscle contractions is interrupted. The protein botulin works in a similar way, causing one of the most dangerous food poisonings, botulism. But the polio virus destroys those nerve fibers through which signals for muscle contractions are sent with the help of calcium, and the muscles, left unused, gradually dry out. On the other hand, this same “calcium drive” can be used for beneficial purposes. So, heart patients need to lower the heart rate, in otherwise under load, it will require more oxygen than the vessels narrowed due to atherosclerosis are able to provide. These people are helped by “β-blockers” - drugs that slightly block calcium channels, thereby lowering calcium levels and, accordingly, reducing the range of contractions of the heart muscle.

Movement within ordinary cells is carried out by other motors, and unlike myosin, their study began in 1985, when Tom Reese and Michael Sheetz discovered the first of them, kinesin. The kinesin molecule is shaped like a myosin molecule - the same rounded heads on a long stalk. With its two heads, the molecule grabs the surface of the microtubule, and a vial of chemicals is attached to the protruding leg. Under the influence of ATP, the molecule bends so that its front head moves a little further from the back and, as a result, grabs a microtubule a little further along the path; then the rear head is again pulled towards the front. This “force push” is then repeated. As a result, the bubble sitting on the stem of the molecule moves jerkily along the microtube. The picture resembles a caterpillar crawling along a branch. Kinesin is capable of transporting vesicles with chemicals necessary for the cell in only one direction - from the center of the cell to its periphery, and dynein moves in the opposite direction. Microtubes have unidirectional block structures built into them (with a “head” and a “tail”). It is not yet clear how the bubbles know which way to move. In 1990, Richard Valley discovered another type of molecular motor, dynamin. Currently, it is believed that in cells there are at least fifty molecules that carry or move cargo, working on a different principle - the transformation of chemical energy into the energy of changing the shape of a flexible molecule, which, due to this change, is able to “grab and intercept” a certain long, inflexible intracellular fiber and “ crawl" along it with a load. In addition, the dynein molecule combines with the energy molecule ATP, something like pulling a bow occurs - the center of the dynein molecule comes forward, and the angle between its ends decreases (like the ends of a bow). Then, after the work has been done, the dynein molecule “straightens,” as it were—a “forceful push” occurs and one end moves relative to the other by 15 nm. Such a mechanism was discovered under the leadership of S. Burgess in 2003 by a group of scientists

Molecules that perform the function of movement in our body (a-kinesin, b-dynein, c-myosin). B) “Molecular motor” of kinesin, with the help of which the molecule transports various substances along microtubules.

The ATP needs of the working muscle are satisfied through the following enzymatic reactions:

1. Reserve in the form of creatine phosphate. Rapid ATP regeneration can be achieved by transferring the phosphate group of creatine phosphate to ADP (ADP) in a reaction catalyzed by creatine kinase. However, this muscle reserve of “high-energy phosphate” is consumed within a few seconds. At rest, creatine phosphate is synthesized again from creatine. In this case, the phosphate group is attached to the guanidine group of creatine (N-guanidino-N-methylglycine). Creatine, which is synthesized in the liver, pancreas and kidneys, is mainly stored in the muscles. Here, creatine is slowly cyclized through a non-enzymatic reaction to form creatinine, which is transported to the kidneys and eliminated from the body.

2 Anaerobic glycolysis. IN muscle tissue The most important long-term energy reserve is glycogen. In resting tissue, the glycogen content is up to 2% of muscle mass. When degraded by phosphorylase, glycogen is easily broken down to form glucose-6-phosphate, which is converted into pyruvate during subsequent glycolysis. With a high need for ATP and insufficient oxygen supply, pyruvate is reduced through anaerobic glycolysis into lactic acid (lactate), which diffuses into the blood.

3. Oxidative phosphorylation. IN aerobic conditions the resulting pyruvate enters the mitochondria, where it undergoes oxidation. Oxidative phosphorylation is the most efficient and constant pathway for ATP synthesis. However, this path is implemented provided there is a good supply of oxygen to the muscles. Along with glucose formed during the breakdown of muscle glycogen, other “energy carriers” present in the blood are also used for the synthesis of ATP: blood glucose, fatty acids and ketone bodies.

4. Formation of inosine monophosphate [IMP]. Another source quick recovery ATP level is the conversion of ADP to ATP and AMP (AMP), catalyzed by adenylate kinase (myokinase). The resulting AMP, due to deamination, is partially converted into IMP (inosine monophosphate), which shifts the reaction in the desired direction.

Of all the methods for ATP synthesis, the most productive is oxidative phosphorylation. Due to this process, the ATP needs of the constantly working heart muscle (myocardium) are met. That's why for successful work heart muscle prerequisite is a sufficient supply of oxygen (myocardial infarction is a consequence of interruptions in the supply of oxygen).

In highly active (red) skeletal muscle, the energy source for ADP rephosphorylation is oxidative phosphorylation in mitochondria. Myoglobin (Mb), a protein similar to hemoglobin that has the property of storing oxygen, takes part in providing these muscles with oxygen. In low-active skeletal muscles, lacking red myoglobin and therefore white, the main source of energy for restoring ATP levels is anaerobic glycolysis. Such muscles retain the ability to rapidly contract, but they can only work a short time, since during glycolysis the formation of ATP occurs at a low yield. Over time, the muscles become exhausted as a result of changes in pH in the muscle cells.

The breakdown of glycogen is controlled by hormones. The process of glycogenolysis is stimulated by adrenaline (via b-receptors) due to the formation of cAMP and activation of phosphorylase kinase. Activation of phosphorylase also occurs with an increase in the concentration of Ca 2+ ions during muscle contraction.

Electromechanical interface is a cycle of sequential processes, starting with the occurrence of an action potential of the AP on the sarcolemma (cell membrane) and ending with the contractile response of the muscle.

Violation of the sequence of pairing processes can lead to pathologies and even death.

The process of cardiomyocyte contraction occurs in the following order:

1) when a stimulating pulse is applied to the cell, fast (activation time 2 ms) sodium channels open, Na + ions enter the cell, causing depolarization of the membrane;

2) as a result of membrane depolarization, voltage-dependent slow calcium channels open (lifetime 200 ms), and Ca 2+ ions come from the extracellular environment, where their concentration is ≈ 2 ∙ 10 3 mol / l, into the cell (intracellular concentration of Ca 2+ ≈10-7 mol/l);

3) calcium entering the cell activates the membrane of the SR, which is an intracellular depot of Ca 2+ ions (in the SR their concentration reaches more than 10 -3 mol/l), and calcium is released from the vesicles of the SR. As a result, a so-called “calcium volley” occurs. Ca 2+ ions from the SR enter the actin-myosin complex of the sarcomere, open the active centers of the actin chains, causing the closure of the bridges and the further development of strength and shortening of the sarcomere;

4) at the end of the process of myofibril contraction, Ca 2+ ions are actively pumped into the sarcoplasmic reticulum using calcium pumps located in the SR membrane;

5) the process of electromechanical coupling ends with the Na + and Ca 2+ - ions being actively released into the extracellular environment using the corresponding ion pumps.

Passive flows 1, 2 and 3 ensure the process of muscle contraction, and active flows 4 and 5 ensure its relaxation.

Experiments have shown that: a) the absence of calcium flow from outside cell I stops the contraction of sarcomeres, b) under conditions of a constant amount of calcium released from the SR, changes in the amplitude of the flow leads to a well-correlated change in the force of contraction. The flow of Ca 2+ ions into the cell thus performs two functions: it forms a long (200 ms) plateau of the action potential of the cardiomyocyte and participates in the process of electromechanical coupling.

3. The purpose of students’ activities in class:

The student must know:

1.Muscle structure.

2. Basic provisions of the sliding thread model.

3. Three-component Hill model.

4.Isometric and isotonic modes for studying the characteristics of contracting muscles.

5.Mechanism of electromechanical coupling in muscles.

The student must be able to:

1. Explain the sliding thread model.

2. Explain Hill's three-component model.

3. Analyze the Hill equation.

4. Explain the process of contraction of cardiomycitis.

5. Solve situational problems on this topic.

1. Muscle structure. Sarcomere.

2. Model of sliding threads.

3. Passive muscle stretching. Hill's three-component model.

4. Active muscle contraction.

5. Hill's equation.

6. Single contraction power.

7. Electromechanical interface.

8. Solving situational problems.

5. List of questions to check the initial level of knowledge:

1. What is the elementary contractile unit of muscle tissue?

2. Describe the microstructure of a sarcomere.

3. What is the mechanochemical energy converter of ATP?

4. How is the process of shortening and force generation carried out in the sarcomere? What are the main principles of the sliding thread model?

5. Why is it necessary to divide the modes of its operation into isotonic and isometric to study the process of muscle contraction? What mode is implemented in real reduction conditions?

6.What is meant by electromechanical coupling? Which phases of electromechanical coupling in the cardiomyocyte and in skeletal muscle are carried out by passive ion flows, and which by active ones?

6. List of questions to check the final level of knowledge:

1. Describe Hill's three-component model.

2. Explain the mechanism of active muscle contraction.

3. Why does isometric contraction have a different shape of the F(t) dependence at different initial muscle lengths?

4. Is it possible to determine from the V(P) Hill curve (Fig. 7) what maximum load a muscle can hold?

5. Describe the process of cardiomycyte contraction.

7. Solve problems:

1. A tendon 16 cm long under the influence of a force of 12.4 N lengthens by 3.3 mm. The tendon can be considered round in cross section with a diameter of 8.6 mm. Calculate the modulus of elasticity of this tendon.

2.Sectional area femur human is equal to 3 cm 2. How much compression force can a bone withstand without collapsing?

3. To determine the mechanical properties of bone tissue, a plate was taken from the calvarium with the following dimensions: length L = 5 cm, width b = 1 cm, thickness h = 0.5 cm. Under the action of a force F = 200 N, the plate lengthened by ∆L = 1.2∙10 -3 cm. Using these data, determine the Young’s modulus of bone tissue under tensile deformation.

4.From tibia The dogs cut out a rectangular rod with edges a = 2 mm, b = 5 mm. The rod was placed on stops located at a distance L = 5 cm from each other, and a force of 28 N was applied to it in the middle between them. In this case, the deflection arrow turned out to be equal to 1.5 mm. Determine Young's modulus for this bone.

8. Independent work of students:

Based on the textbook by Antonov V.F. and others (§§ 20.4.) study the time relationship between the cardiomycyte action potential and a single contraction.

9. Chronocard training session:

1. Organizational moment – 5 min.

2. Analysis of the topic – 30 min.

3. Solving situational problems – 60 min.

4. Current knowledge control – 30 min

5. Summing up the lesson – 10 min.

10. List educational literature to the lesson:

1.Remizov A.N. Maksina A.G., Potapenko A.Ya. Medical and biological physics. M., Bustard, 2008, §§ 8.3, 8.4.

The molecular mechanism of muscle contraction through the sliding of actin filaments is as follows. Myosin heads connect the protofibril to the actin fibril. When they tilt, sliding occurs, moving the actin filament towards the center of the sarcomere. Due to the bipolar organization of myosin molecules on both sides of the filaments, conditions are created for actin filaments to slide in different directions.

The main thing in the theory is that it is not the filaments (myosin and actin) that are shortened. Their length remains unchanged even when the muscles are stretched. But bundles of thin threads, slipping, come out between thick threads, the degree of their overlap decreases, and thus contraction occurs.

Regulatory role of calcium ions in muscle contraction

As mentioned above, for skeletal muscle contraction to occur, calcium ions must enter the myofibrils from the sarcoplasmic reticulum. This is the name given to the system of vesicles and cisterns separated by membranes from the rest of the sarcoplasm (Figure 6). The SPS occupies approximately 10% of the volume of the muscle fiber, and the total area of its membranes in the myocyte is approximately 100 times larger than the surface of the sarcolemma (sarcomere membrane). ATP serves as a calcium depot in muscle fiber - the content of calcium ions in it is enormous. Consequently, a colossal Ca 2+ gradient is maintained on the SPS membrane, but at rest it is completely impenetrable to this ion.

The release of calcium from the SPS stops immediately following the repolarization of the sarcolemma, but the myofibrils remain in a contracted state. In order for the myofibrils to relax, calcium must return back to the sarcoplasmic reticulum. But such transport has to be carried out despite the action of a huge concentration gradient (there is a lot of calcium in the SPS, but little in the sarcoplasm). Consequently, relaxation of myofibrils in the skeletal muscle myocyte after their contraction is impossible without the participation of the active transport system - the calcium pump (Figure 6, B). Its work is an integral element of the contractile process in the muscle. A Ca-activated ATPase, which serves as the main component of the calcium pump, was isolated from the SPS membrane.

Chemomechanical stage of muscle contraction

At rest, when there are few Ca ions, sliding does not occur, because this is prevented by troponin molecules and the negative charges of ATP, ATPase and ADP. The increased concentration of Ca ions occurs due to its entry from the interfibrillar space. In this case, a number of reactions occur with the participation of Ca ions:

The decrease in the performance of a muscle isolated from the body during prolonged irritation is due to two main reasons. The first of them is that during contractions, metabolic products accumulate in the muscle (phosphoric acid, Ca++ binding, lactic acid, etc.), which have a depressing effect on muscle performance. Some of these products, as well as Ca ions, diffuse from the fibers out into the pericellular space and have a suppressive effect on the ability of the excitable membrane to generate AP. So, if isolated muscle placed in a small volume of Ringer's fluid until complete fatigue, then it is enough to just change the solution washing it to restore muscle contractions.

Mechanism of muscle contraction

It is calculated that each myofibril, whose diameter is 1 μm, contains approximately 2500 protofibrils, that is, elongated polymerized protein molecules (actin and myosin). Actin protofibrils are twice as thin as myosin protofibrils. At rest, these muscles are located in such a way that the actin filaments with their tips penetrate into the spaces between the myosin protofibrils.

Electron microscopy shows that on the sides of the myosin filament there are protrusions called cross bridges. They are oriented relative to the axis of the myosin filament at an angle of 120°. According to modern concepts, the transverse bridge consists of a head and a neck. The head acquires pronounced ATPase activity upon binding to actin. The neck has elastic properties and is a hinged joint, so the head of the cross bridge can rotate around its axis.

Electromechanical coupling in muscles

Electromechanical coupling in cardiac muscle

Stage 2. ATP hydrolysis. The breakdown of ATP into ADP and inorganic phosphate (P) occurs in the myosin head, the hydrolysis products remain in the myosin. As a result of hydrolysis, the myosin head “straightens,” i.e. located perpendicularly or at an angle of 90 0 relative to thick and thin threads. This movement causes the tip of the myosin filament to move 11 nm along the actin filament and the myosin head to face the new actin monomer. If all the cross bridges are in this state, the muscle is relaxed.

2. Cardiac glycosides. Digitalis derivatives are capable of inhibiting the plasma membrane Na-K pump and consequently increasing intracellular Na + levels (i). As a result, Na-Ca metabolism slows down, [Ca 2+ ] i levels increase, and contractility increases. Recent studies have revealed a new mechanism of action of cardiac glycosides - through an increase in the permeability of Na + channels of the plasma membrane for Ca 2+ ions.

Neuromuscular physiology

Quantum hypothesis of mediator release. Postsynaptic potentials evoked by motor nerve stimulation (end plate potentials - EPPs) vary in amplitude from stimulus to stimulus, and these fluctuations are a multiple of the MEPP amplitude. It was assumed that the transmitter in the synapse is released in the form of multimolecular portions - quanta. At rest, the random release of individual portions from the nerve ending causes the appearance of MEPPs on the postsynaptic membrane, and in response to irritation, the synchronous release of several tens or hundreds of quanta occurs and PEP appears. Electrophysiological determination showed that the transmitter quantum consists of 1000-10,000 acetylcholine molecules.

Comedians are co-occurring synaptic messengers characterized primarily by co-localization, co-release, and a common target cell. Co-localization refers to the synthesis and deposition of transmitters in the same neuron, their origin in the same presynaptic terminals, but not necessarily in the same vesicles. Co-release refers to the exocytosis of two (or more) transmitters as a result of the same activation of the presynaptic terminal, which in this case does not mean a single presynaptic action potential, but a discharge of action potentials with the same frequency.

The mechanism of electromechanical coupling, slip theory, and the role of calcium ions

This activation mechanism is due to the action of Ca 2+ on troponin, which works as "calcium switch": when binding to Ca 2+, its molecule is deformed in such a way that it seems to push tropomyosin into the groove between the two chains of actin monomers, i.e., into the “activated position.”

Smooth muscle cells are spindle-shaped, approximately 50–400 µm long and 2–10 µm thick. United by special intercellular contacts (desmosomes), they form a network with collagen fibers woven into it. Due to the irregular distribution of myosin and actin filaments, these cells lack the transverse striation characteristic of cardiac and skeletal muscles. They are also shortened due to the sliding of myofilaments relative to each other, but the rates of sliding and ATP breakdown here are 100–1000 times lower than in striated muscles. In this regard, smooth muscles are especially well adapted for long-term sustainable contraction, which does not lead to fatigue and significant energy consumption. The contractile tension per unit cross-sectional area is often the same in smooth and skeletal muscles (30–40 N/cm2), and during prolonged contraction they can support the same load. However, the energy consumed in this smooth muscle, if assessed by O 2 consumption, 100–500 times less.

Biology and medicine

A separate system consists of transverse tubules (T-tubules), which cross the muscle fiber at the border of the A-discs and I-discs, pass between the lateral cisterns of two adjacent sarcomeres and emerge on the surface of the fiber, forming a single whole with the plasma membrane. The lumen of the T-tubule is filled with extracellular fluid surrounding the muscle fiber. Its membrane, like the plasma membrane, is capable of conducting an action potential. Having arisen in the plasma membrane, the action potential quickly spreads along the surface of the fiber and the membrane of the T-tubules deep into the cell. Having reached the region of the T-tubules adjacent to the lateral cisterns, the action potential activates the voltage-dependent “gate” proteins of their membranes, which are physically or chemically coupled to the calcium channels of the membrane of the lateral cisterns. Thus, depolarization of the T-tubule membrane. caused by the action potential, leads to the opening of calcium channels in the membrane of the lateral cisterns containing Ca2+ in high concentrations, and Ca2+ ions enter the cytoplasm. An increase in cytoplasmic Ca2+ levels is usually sufficient to activate all muscle fiber cross bridges.

The contraction process continues as long as Ca2+ ions are bound to troponin, i.e. until their concentration in the cytoplasm returns to its original low value. The membrane of the sarcoplasmic reticulum contains Ca2+-ATPase, an integral protein that actively transports Ca2+ from the cytoplasm back into the cavity of the sarcoplasmic reticulum. Ca2+ is released from the reticulum as a result of action potential propagation along the T-tubules; it takes much longer to return to the reticulum than to exit. Therefore, the increased concentration of Ca2+ in the cytoplasm persists for some time and muscle fiber contraction continues after the end of the action potential.

MECHANISM OF MUSCLE FIBER CONTRACTION

3. The process takes place electromechanical interface: it represents the conversion of an electrical action potential into mechanical “sliding” of protofibrils relative to each other. This process occurs in several stages with the obligatory means of ions calcium!

Storage and release of calcium ions. In a state of relaxation, the muscle contains more 1 µmol Ca per 1 g wet weight. If Ca salts were not isolated in special intracellular stores enriched with calcium muscle fibers would be in a state of continuous contraction. The structure of intracellular calcium storage systems is as follows: in many areas, the muscle cell membrane goes deep into the fiber, perpendicular to its longitudinal axis, forming tubes; this system of transverse tubes (T-system) connects with the extracellular environment. Perpendicular to the T-system, i.e. parallel to the myofibrils, there is a system of longitudinal tubules (true sarcoplasmic reticulum). Bubbles at the ends of these tubes, terminal tanks , are very close to the membranes of the transverse system, forming triads. Intracellular Ca 2+ is stored in these vesicles. Unlike the transverse system, the longitudinal system is not connected to the environment.

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