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The synapse or connection between a motor neuron and a skeletal muscle is known as neuromuscular junction. Communication happens between the neuron and muscle via nerve cells. Due to this communication or transmission of signal, the muscle is able to contract or relax. It is the most widely studied synapse and it is comparatively easier to understand and analyze as well. We shall look in detail about the junction, what it consists of, what are its functions as well as some disorders associated with the junction.
A motor neuron is responsible for causing a skeletal muscle to contract, by stimulating it. The gap or space present between this motor neuron and the skeletal muscle cell is called as a synapse. This synapse, specifically between the skeletal muscle cell and motor neuron is called neuromuscular myoneural or junction. Myo means Muscle and Neural means Nerves. When an impulse travels between this space, muscle contraction happens.
There are around trillion such connections in the human brain, between two nerves or nerves and glands. In this article we will discuss only the junction.
As we have read, the junction consists of a neuron and a skeletal muscle cell. The neuron in the combination is referred to as spinal motor neuron. The motor neurons, who originate from the spinal cord, innervate the skeletal muscle fibers. The innervation happens by very fine processes of the axon. The synapses are present along these processes and are also known as motor endplate, because of its specific structure.
Before going in detail, let us remember the broad action of this junction. It is to act like a bridge between a neuron and muscle cell to transmit the signals. However, aerobic respiration does not synthesize ATP as quickly as anaerobic glycolysis, meaning that the power output of muscles declines, but lower-power contractions can be sustained for longer periods.
Muscles require a large amount of energy, and thus require a constant supply of oxygen and nutrients. Blood vessels enter muscle at its surface, after which they are distributed through the entire muscle. Blood vessels and capillaries are found in the connective tissue that surrounds muscle fascicles and fibers, allowing oxygen and nutrients to be supplied to muscle cells and metabolic waste to be removed.
Myoglobin, which binds oxygen similarly to hemoglobin and gives muscle its red color, is found in the sarcoplasm. This combination of different energy sources is important for different types of muscle activity. As an analogy, a cup of coffee with lots of sugar provides a quick burst of energy but not for very long. A balanced meal with complex carbohydrates, protein and fats takes longer to impact us, but provides sustained energy.
After the first few seconds of exercise, available ATP is used up. After the next few minutes, cellular glucose and glycogen are depleted. After that time, fatty acids and other energy sources are used to make ATP. Sometimes, time is important. You have already learned about the anatomy of the sarcomere,with its coordinated actin thin filaments and myosin thick filaments. For a muscle cell to contract, the sarcomere must shorten in response to a nerve impulse.
The thick and thin filaments do not shorten, but they slide by one another, causing the sarcomere to shorten while the filaments remain the same length. This process is known as the sliding filament model of muscle contraction. The mechanism of contraction is accomplished by the binding of myosin to actin, resulting in the formation of cross-bridges that generate filament movement.
When a sarcomere shortens, some regions shorten while others remain the same length. A sarcomere is defined as the distance between two consecutive Z discs or Z lines. When a muscle contracts, the distance between the Z discs is reduced. The H zone, the central region of the A zone, contains only thick filaments and shortens during contraction. The I band contains only thin filaments and also shortens.
The A band does not shorten; it remains the same length, but A bands of adjacent sarcomeres move closer together during contraction. Thin filaments are pulled by the thick filaments towards the center of the sarcomere until the Z discs approach the thick filaments.
The zone of overlap, where thin filaments and thick filaments occupy the same area, increases as the thin filaments move inward. The ideal length of a sarcomere to produce maximal tension occurs when all of the thick and thin filaments overlap. If a sarcomere is stretched past this ideal length, some of the myosin heads in the thick filaments are not in contact with the actin in the thin filaments, and fewer cross-bridges can form.
This results in fewer myosin heads pulling on actin, and less tension is produced. If a sarcomere is shortened, the zone of overlap is reduced as the thin filaments reach the H zone, which is composed of myosin tails.
Because myosin heads form cross-bridges, actin will not bind to myosin in this zone, again reducing the tension produced by the muscle. If further shortening of the sarcomere occurs, thin filaments begin to overlap with each other, further reducing cross-bridge formation and the amount of tension produced.
If the muscle were stretched to the point where thick and thin filaments do not overlap at all, no cross-bridges are formed, and no tension is produced. This amount of stretching does not usually occur, as accessory proteins and connective tissue oppose extreme stretching. With large numbers of relatively weak molecular motors, we can more easily adjust the force to meet our needs. Otherwise, we would regularly be producing too little or too much force for most of our tasks.
Also, molecules are only capable of generating small forces based on their molecular structure. You have already learned about how the information from a neuron ultimately leads to a muscle cell contraction.
One action potential in a motor neuron produces one contraction. This contraction is called a twitch. A single twitch does not produce any significant muscle contraction. Multiple action potentials repeated stimulation are needed to produce a muscle contraction that can produce work. A twitch can last from a few milliseconds up to milliseconds, depending on the muscle type. The tension produced by a single twitch can be measured by a myogram, which produces a graph illustrating the amount of tension produced over time.
When combined with a plot of electrical signaling, the myogram shows three phases that each twitch undergoes. No tension or contraction is produced at this point, but the conditions for contraction are being established.
This is the phase during which excitation and contraction are being coupled but contraction has yet to occur. The contraction phase occurs after the latent period when calcium is being used to trigger cross-bridge formation.
This period lasts from the beginning of contraction to the point of peak tension. The last phase is the relaxation phase, when tension decreases as contraction stops. Calcium is pumped out of the sarcoplasm, back into the SR, and cross-bridge cycling stops. The muscle returns to a resting state. There is a very short refractory period after the relaxation phase Review the previous material about the physiology of a neuromuscular junction.
A single twitch does not produce any significant muscle activity in a living body. Normal muscle contraction is more sustained, and it can be modified to produce varying amounts of force. This is called a graded muscle response. The tension produced in a skeletal muscle is a function of both the frequency of neural stimulation and the number of motor neurons involved.
The rate at which a motor neuron delivers action potentials affects the contraction produced in a muscle cell. If a muscle cell is stimulated while a previous twitch is still occurring, the second twitch will not have the same strength as the first; it will be stronger. This effect is called summation, or wave summation, because the effects of successive neural stimuli are summed, or added together.
This allows for more cross-bridge formation and greater contraction. Because the second stimulus has to arrive before the first twitch has completed, the frequency of stimulus determines whether summation occurs or not.
If the frequency of stimulation increases to the point at which each successive stimulus sums with the force generated from the previous stimulus, muscle tension continues to rise until the tension generated reaches a peak point.
The tension at this point is about three to four times higher than the tension of a single twitch; this is referred to as incomplete tetanus. Tetanus is defined as continuous fused contraction. During incomplete tetanus, the muscle goes through quick cycles of contraction with a short relaxation phase. If the stimulus frequency is so high that the relaxation phase disappears completely, contractions become continuous in a process called complete tetanus. This contraction continues until the muscle fatigues and can no longer produce tension.
This type of tetanus is not the same as the disease of the same name that is distinguished by severe sustained contraction of skeletal muscles. The disease, which can be fatal if left untreated, is caused by the bacterium Clostridium tetani , which is present in most environments.
Slightly different from incomplete tetanus is the phenomenon of treppe. Treppe from the German term for step, referring to stepwise increases in contraction is a condition in which successive stimuli produce a greater amount of tension, even though tension goes back to the resting state between stimuli in tetanus, tension does not decrease to the resting state between stimuli.
Treppe is similar to tetanus in that the first twitch releases calcium into the sarcoplasm, some of which will not be taken back up before the next contraction. Each stimulus afterward releases more calcium, but there is still some calcium present in the sarcoplasm from the previous stimulus. This extra calcium permits more cross-bridge formation and greater contraction with each additional stimulus up to the point where added calcium cannot be utilized.
At this point, successive stimuli will produce a uniform amount of tension. The strength of contractions is controlled not only by the frequency of stimuli but also by the number of motor units involved in a contraction. A motor unit is defined as a single motor neuron and the corresponding muscle fibers it controls. These drugs are powerful agonists of the nicotinic receptors. They cause excessive depolarization, that cannot be reversed. The prolonged depolarization causes A1 block, resulting in relaxation of skeletal muscles.
These include suxamethonium and other drugs. The important clinical conditions associated with the neuromuscular junction are as follows.
It is an autoimmune disease in which antibodies are formed against the acetylcholine receptors. As a result, the neuromuscular junction is unable to initiate the contraction of skeletal muscles. It results in varying degrees of muscle weakness. The most commonly affected muscles include the muscle of eyes, face and the pharynx that assist in swallowing.
It is another autoimmune disease of the neuromuscular junction. However, it affects the presynaptic neurons. In this disease, antibodies are formed against the voltage-gated calcium channels present on the presynaptic neurons. The muscles are unable to contract.
It also causes varying degrees of skeletal muscle weakness. The most commonly affected muscles include those of legs and arms. The person feels difficulty in walking, climbing stairs, etc. This disease of the neuromuscular junction results in hyperexcitation of the skeletal muscles. It is due to the downregulation of postsynaptic voltage-gated potassium channels.
As a result, the potassium ions are unable to leave the skeletal muscle and hyperpolarization occurs. This hyperpolarization leads to the hyperexcitation of skeletal muscle and muscle spasms. It is also believed to be an autoimmune disorder of the neuromuscular junction. Neuromuscular junction is a microstructure present at the junction of motor neurons and the skeletal muscle fibers.
It acts as a bridge connecting the skeletal system and the nervous system. The presynaptic terminal is the axonal terminal of motor neuron containing synaptic vesicles. The postjunctional sarcolemma has the synaptic clefts having acetylcholine receptors on their walls. The acetylcholine molecules released by the presynaptic terminal bind to these receptors and cause the opening of the cation channels. The sodium ions diffuse through these channels, resulting in depolarization od skeletal muscles.
This depolarization initiates the process of muscle contraction. The acetylcholine is soon metabolized by the acetylcholinesterase, which eliminates all its effects. The normal mechanism of neuromuscular junction is affected by cholinergic drugs as well as skeletal muscle relaxants.
The cholinergic drugs , which may be direct-acting or indirect-acting, increase the activity of acetylcholine. The skeletal muscle relaxants are the neuromuscular blockers. The block the neuromuscular junction by inhibiting the depolarization or by causing excessive depolarization. All these are autoimmune conditions.
The first two result in muscle weakness while the third one causes hyperextension of skeletal muscles.
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