Site where motor neuron and muscle fiber meet

Motor unit - Wikipedia

site where motor neuron and muscle fiber meet

This is an experimental portion of the website. Each keyword starts a A motor unit is defined as the neuron and the fibers it supplies. Cardiac muscle sarcoplasm has a great amount of mitochondria to meet the energy demands. Similar to. A motor unit is made up of a motor neuron and the skeletal muscle fibers innervated by that .. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc. The process of muscle contraction begins at the site where a motor neuron's terminal meets the muscle fiber—called the neuromuscular junction (NMJ).

Skeletal Muscle Skeletal muscle is mainly responsible for the movement of the skeleton, but is also found in organs such as the globe of the eye and the tongue.

It is a voluntary muscle, and therefore under conscious control.

Upper motor neurons (video) | Khan Academy

Skeletal muscle is specialized for rapid and forceful contraction of short duration. Skeletal muscle cells contain similar components and structures as other cells but different terms are used to describe those components and structure in skeletal muscle cells. The plasma membrane of skeletal muscle is called the sarcolemma; its cytoplasm is known as sarcoplasm; the endoplasmic reticulum is called the sarcoplasmic reticulum.

  • Motor neurons
  • Motor unit
  • The Neuromuscular Junction

Each muscle cell is defined by a sarcolemma and contains many nuclei along its length. The nuclei are displaced peripherally within a cross section of the sarcoplasm while a large number of longitudinal myofibrils, groups of arranged contractile proteins, occupy most of the center space.

The myofibril contains several important histological landmarks: The myofibril is composed of alternating bands. The I-bands isotropic in polarized light appear light in color and the A-bands anisotropic in polarized light appear dark in color.

site where motor neuron and muscle fiber meet

The alternating pattern of these bands results in the striated appearance of skeletal muscle. The Z-lines Zwischenschieben bisect the I-bands. A light band called the H-band Heller sits within each A-band.

The M-line Mittelschiebe bisects each A-band and, in doing so, bisects each H-band. Each myofibril can be understood as a series of contractile units called sarcomeres that contains two types of filaments: The individual filaments do not change in length during muscle contraction; rather the thin filaments slide over the thick filaments to shorten the sarcomere.

The nature of these filaments can be understood in the context of the histological landmarks of the myofibril. The thick filaments are a bipolar array of polymerized myosin motors. The motors on one side of the filament are oriented in the same direction whereas the motors on the other side of the filament are oriented in the opposite direction. The center of the filament lacks motors; it contains only the coiled-coil region of the myosins.

A set of proteins crosslinks each myosin filament to its neighbors at the center of the filament. These proteins make up the M-line. The thin filaments are attached to a disc-like zone that appears histologically as the Z-line. The Z-lines contain proteins that bind and stabilize the plus ends of actin filaments.

Z-lines also define the borders of each sarcomere. The I- and H-bands are areas where thick and thin filaments do not overlap this is why these bands appear paler under the microscope.

The I-band exclusively contains thin filaments whereas the H-band contains exclusively thick filaments.

Upper motor neurons

Skeletal muscles are divided into two muscle fiber types: Slow-twitch type I muscle fibers contract more slowly and rely on aerobic metabolism. They contain large amounts of mitochondria and myoglobin, an oxygen-storage molecule.

The reddish color of myoglobin is why these fibers may be referred to as red fibers. These muscles can maintain continuous contraction and are useful in activities such as the maintenance of posture. Fast-twitch type II muscle fibers contract more rapidly due to the presence of a faster myosin.

site where motor neuron and muscle fiber meet

Type II fibers can be subdivided into those that have large amounts of mitochondria and myoglobin and those that have few mitochondria and little myoglobin.

The former primarily utilize aerobic respiration to generate energy, whereas the latter rely on glycolysis. The lack of myoglobin results in a paler color than the slow-twitch muscles, and fast-twitch fibers may therefore be referred to as white fibers.

These muscles are important for intense but sporadic contractions; for example, those that take place in the biceps.

Most muscles contain a mixture of these extreme fiber types. In humans, the fiber types cannot be distinguished based on gross examination, but require specific stains or treatments to differentiate the fibers. A motor unit is defined as the neuron and the fibers it supplies. Some motor neurons innervate one or a few muscle cells whereas other motor neurons can innervate hundreds of muscle cells.

Muscles that require fine control have motor neurons that innervate fewer muscle cells; muscles that participate in less controlled movements may have many fibers innervated by each neuron.

Motor axons terminate in a neuromuscular junction on the surface of skeletal muscle fibers. The neuromuscular junction is composed of a pre-synaptic nerve terminal and a post-synaptic muscle fiber.

Upon depolarization, the pre-synaptic vesicles containing the neurotransmitter acetylcholine fuse with the membrane, releasing acetylcholine into the cleft. Such neurotoxins do not respond well to anti-venoms. After one hour of inoculation of these toxins, including notexin and taipoxinmany of the affected nerve terminals show signs of irreversible physical damage, leaving them devoid of any synaptic vesicles.

This prevents interaction between the acetylcholine released by the presynaptic terminal and the receptors on the postsynaptic cell.

In effect, the opening of sodium channels associated with these acetylcholine receptors is prohibited, resulting in a neuromuscular blockade, similar to the effects seen due to presynaptic neurotoxins. This causes paralysis in the muscles involved in the affected junctions. Unlike presynaptic neurotoxins, postsynaptic toxins are more easily affected by anti-venoms, which accelerate the dissociation of the toxin from the receptors, ultimately causing a reversal of paralysis.

These neurotoxins experimentally and qualitatively aid in the study of acetylcholine receptor density and turnoveras well as in studies observing the direction of antibodies toward the affected acetylcholine receptors in patients diagnosed with myasthenia gravis. Neuromuscular junction disease Any disorder that compromises the synaptic transmission between a motor neuron and a muscle cell is categorized under the umbrella term of neuromuscular diseases.

These disorders can be inherited or acquired and can vary in their severity and mortality. In general, most of these disorders tend to be caused by mutations or autoimmune disorders. Autoimmune disorders, in the case of neuromuscular diseases, tend to be humoral mediated, B cell mediated, and result in an antibody improperly created against a motor neuron or muscle fiber protein that interferes with synaptic transmission or signaling.

In seronegative myasthenia gravis low density lipoprotein receptor-related protein 4 is targeted by IgG1which acts as a competitive inhibitor of its ligand, preventing the ligand from binding its receptor. It is not known if seronegative myasthenia gravis will respond to standard therapies. MG can be transferred from the mother to the fetus by the movement of AChR antibodies through the placenta. Signs of this disease at birth include weakness, which responds to anticholinesterase medications, as well as fetal akinesia, or the lack of fetal movement.

Neuromuscular junction

This form of the disease is transient, lasting for about three months. However, in some cases, neonatal MG can lead to other health effects, such as arthrogryposis and even fetal death.

This rare disease can be marked by a unique triad of symptoms: Examples of autonomic dysfunction caused by LEMS include erectile dysfunction in men, constipationand, most commonly, dry mouth. Less common dysfunctions include dry eyes and altered perspiration.

Areflexia is a condition in which tendon reflexes are reduced and it may subside temporarily after a period of exercise. This type of tumor also expresses voltage-gated calcium channels. In the US, treatment with 3,4-diaminopyridine for eligible LEMS patients is available at no cost under an expanded access program. Rather than causing muscle weakness, NMT leads to the hyperexcitation of motor nerves.

site where motor neuron and muscle fiber meet

NMT causes this hyperexcitation by producing longer depolarizations by down-regulating voltage-gated potassium channelswhich causes greater neurotransmitter release and repetitive firing. This increase in rate of firing leads to more active transmission and as a result, greater muscular activity in the affected individual.