Muscle Fiber Essay

Muscle contraction can be understood as the consequence of a process of transmission of action potentials from one neuron to another. A chemical called acetylcholine is the neurotransmitter released from the presynaptic neuron. As the postsynaptic cells on the muscle cell membrane receive the acetylcholine, the channels for the cations sodium and potassium are opened. These cations produce a net depolarization of the cell membrane and this electrical signal travels along the muscle fibers. Through the movement of calcium ions, the muscle action potential is taken into actual muscle contraction with the interaction of two types of proteins, actin and myosin.

Next, to determine if contraction via the EMC pathway requires extracellular or intracellular calcium, the second type of stimulus was used and the tissue was stimulated using calcium free K+-depolarising solution. The bathing solution in this experiment was calcium free solution to make sure all extracellular calcium was eliminated, as without calcium, the EMC pathway is expected to produce no response.

Muscle fibres, as shown in Diagram 1, consist of myofibrils, which contain the proteins, actin and myosin, in specific arrangements . The diagram illustrates how a muscle is made up of many fascicles, which in turn are made up of many endomysiums, and within them, many muscle fibres. Each muscle fibre is made up of many myofibrils that consist of sarcomeres bound end on end . Actin is a thin filament, about 7nm in diameter, and myosin is a thick filament, about 15nm in diameter , both of which reside in the sarcomere. They are held together by transverse bands known as Z lines . Diagram 2 shows actin and myosin filaments within a sarcomere, and the Z lines that connect them.

Myofibrils are made up of long proteins that include myosin, titin, and actin while other proteins bind them together. These proteins are arranged into thin and thick filaments that are repetitive along the myofibril in sectors known as sarcomeres. The sliding of actin and myosin filaments along each other is when the muscle is contracting. Dark A-bands and light I-bands reappear along myofibrils. The alignment of myofibrils causes an appearance of the cell to look banded or striated. A myofibril is made up of lots of sarcomeres. As the sarcomeres contract individually the muscle cells and myofibrils shorten in length. The longitudinal section of skeletal muscle exhibits a unique pattern of alternating light and dark bands. The dark staining, A-bands possess a pale region in the middle called the H-zone. In the middle of the H-zone the M-line is found, that displays filamentous structures that can join the thick filaments. The light-staining bands also known as I-bands are divided by thin Z-line. These striated patterns appear because of the presence of myofibrils in the sarcoplasm (IUPUI, 2016).

As stated by (Muscles, 2015) “If a muscle cell fires an action potential, which is as a result of the motor neuron command. Then it causes the release of calcium ions, which are released from the sarcoplasmic reticulum” Sarcoplasmic reticulum is a specialised type of smooth ER that regulates the calcium ion concentration in the cytoplasm of striated muscle cells (Sarcoplasmic Reticulum Cell Biology, 2015).

Muscles owe their ability to contract to structural units called sarcomeres, and a single muscle fiber can contain many thousands of these structures, aligned one next to the other. Each mature sarcomere is made up of precisely arranged and intertwined thin filaments of actin and thicker bundles of motor proteins, surrounded by other proteins. Sliding the motors along the filaments provides the force needed to contract the muscle. However, it was far from clear how sarcomeres, especially the arrays of thin-filaments, are assembled from scratch in developing muscles.

In MG, the postsynaptic muscle membrane is distorted and simplified, having lost its normal folded shape, the concentration of acetylcholine receptors on the muscle

Although both studies used the presence of markers such as horseradish peroxide to identify the membrane during the stimulation of a frog neuromuscular junction; the first of the papers by Heuser and Reese found that portions of cellular membrane at the frog neuromuscular junction were taken up by the cell and converted back into synaptic vesicles whereas ceccarelli observed no vesicle depletion but an increase in the number of labelled vesicles over time. He and his co workers propsed that vesicle fusion involves the opening of a small pore, termed ‘fusion pore’ followed by its rapid closure without full dilation and collapse at the same site of fusion. (reese, n.d.) (cecerlli, n.d.) This composes the Kiss and Run Argument but the electron microscope evidence is neither compelling or persuasive as the images are unclear where the omega membrane profile in the fixed tissue is on the way to collapsing into the plasma membrane or to closing its

Voltage-gated calcium channels function in many ways, one of the most important of which is its role in stimulating the release of vesicles containing the neurotransmitter acetylcholine into the neuromuscular junction. As an action potential reaches the terminus of the neuron, voltage-gated calcium channels are opened causing an influx of calcium into the presynaptic terminal. Acetylcholine filled vesicles, in response to the increase in calcium concentration, fuse to the plasma membrane releasing acetylcholine into the neuromuscular junction. When released in sufficient quantities at neuromuscular junctions acetylcholine binds to post synaptic receptors on the muscle cells and causes contraction of the muscle. If this delicate system

As per the sliding fiber hypothesis, the myosin thick fibers of muscle strands slide past the actin thin fibers amid muscle compression, while the two gatherings of fibers stay at generally steady length.a new idea called cross-connect hypothesis traditionally swinging cross-connect, now for the most part alluded to as cross-connect cycle which clarifies the atomic system of sliding fiber. Cross-connect hypothesis expresses that actin and myosin frame a protein complex traditionally called actomyosin by connection of myosin head on the actin fiber, accordingly shaping a kind of cross-connect between the two fibers. These two corresponding speculations ended up being the right depiction, and turned into a generally acknowledged clarification

Neuromuscular junctions play a key role in skeletal muscle contractions, and they consist of axon terminals, synaptic clefts, and junctional folds. The contraction begins with the arrival of a nerve impulse at an axon terminal which causes acetylcholine (ACh) to be released into the synaptic cleft. ACh then diffuses across the synaptic cleft and binds with receptors on the sarcolemma of skeletal muscles. This binding creates electrical events that allow an action potential through muscle fiber which causes a muscle contraction. However, normal communication between a muscle and nerve can be interrupted due to the neurological disorder, myasthenia gravis. In Latin and Greek, Myasthenia gravis means “grave muscle weakness,” (fact sheet). As stated

form of myosin ATP and are not very good at delivering calcium to the muscle

Microscopical techniques have been an irreplaceable source of our knowledge about the nervous system. Not only have they provided clear evidence supporting the variety of hypotheses but also deepened our understanding by allowing the researchers to make valid links between the components of the nervous system and their functions. In this paper,

Microscopical techniques have been an irreplaceable source of our knowledge about the nervous system. Not only have they provided clear evidence supporting the variety of hypotheses but also deepened our understanding by allowing the researchers to make valid links between the components of the nervous system and their functions. In this paper,

2. Charge, S. B. P., and Rudnicki, M.A. (2004). Cellular and molecular regulation of muscle regeneration. Physiological Reviews, Volume 84, 209-238.