Myasthenia gravis is a disorder that causes muscle fatigue or weakness. This disrupts the normal physiology of a muscle contraction by producing antibodies that attack acetylcholine receptors and damage them. Because of this damage acetylcholine cannot bind to those receptors and the action potential that was initiated cannot move from the neuron to the muscle cell. This disorder will then prevent the contraction of the muscle.
¶ … Muscular System
The normal anatomy and physiology of a muscle determines its capability of formulating a contraction. The contraction of a muscle is dependent on the ability of a neuron to become excited through a process that includes a concentrated flow of sodium (Na+), potassium (K+), and calcium (Ca+) through the neuron and eventually into the muscle cell (Tortora & Derrickson, 2011). A neuron begins its resting membrane potential at -70mv. In order for an action potential to occur, which is the event that will precede the muscle contraction, the membrane must first depolarize and become more positive, reaching -55mv. Once -55mv is reached, the membrane is said to be at the threshold potential, the voltage by which most Na+ channels in the cell membrane would open. After the first Na+ channel opens, the cell becomes even more depolarized and Na+ ions move into the cell (Martini, Nath, & Bartholomew, 2011).
As further depolarization is occurring, more Na+ channels open along the neuron causing the one following it to open, but making the ones behind it that already are open completely unable to perform any activity. Eventually the part of the neuron where the action began reaches a level of 0mv to +30mv, a range where K+ channels can open (Tortora & Derrickson, 2011). The same process occurs concerning the K+ channels as with the Na+ channels, allowing K+ back into the cell, until the cell completely hyperpolarizes, reaching -70mv and ending the action potential, with the mobile Na+ and K+ ions transitioned back to their respective spaces by the sodium-potassium pump (Tortora & Derrickson, 2011).
On the larger scale, the action potential began in the spinal cord in a region where Na+ concentration was high. As the process described already, the signal proceeds down multiple neurons to the skeletal muscle in the legs, those muscles are depolarized, but this time to allow for the opening of Ca+ channels. The release of calcium ions at the neuromuscular junction between the neuron and the skeletal muscles leads to vesicles containing acetylcholine to be released and those will travel to the plasma membrane and exocytose, releasing the acetylcholine into the synaptic space between the cells (Martini, Nath, & Bartholomew, 2011). Acetylcholine binds to ligand receptors on the skeletal muscle membrane, opening and allowing Na+ ions to flow into the cell. The depolarization and generation of an action potential occurs as the cell membrane reaches threshold. The action potential is fully propagated as voltage-gated Na+ channels open and Na+ ions flow into the cell, and cell communication continues throughout the skeletal muscle (Martini, Nath, & Bartholomew, 2011).
During the process of the action potential flowing through the skeletal muscle, Ca+ channels in the sarcoplasmic reticulum open to allow the flow of Ca+ which bind to Troponin C, a protein linked to tropomyosin, both of which are associated overarchingly with actin (Martini, Nath, & Bartholomew, 2011). The binding of Ca+ to troponin C. causes a conformational change in the protein, moving tropomyosin away from the actin-myosin binding site. Without tropomyosin, myosin is free to bind to actin, and can now function as an ATPase and cleave ATP into ADP and Pi (free phosphorus). After being attached for some time, Pi detaches from the myosin head, causing a conformational change in the form of a 45o bend. This is the full power stroke, translating into what is seen and referred to as a muscle contraction. ADP eventually diffuses, resulting in myosin binding with a new ATP molecule and allowing for the detachment of the myosin head from actin, and allowing for the contracted muscle to relax (Tortora & Derrickson, 2011).
As a full muscle contraction comes to an end, it will restart if the conditions are ideal. However, any deviation from normal activity can have severe consequences, as with the disease Myasthenia gravis. Myasthenia gravis disrupts the normal cycle of a muscle contraction and causes muscle fatigue or weakness. As a result of this illness antibodies are produced that end up binding to the acetylcholine receptors, which ultimately causes the destruction of the receptor and eventually leads to a reduction in the number of available and functional receptors (Chabner, 2011). Because of this, acetylcholine is unable to bind and accumulates. However, acetylcholine is necessary in order to initiate a contraction. If there is no binding of the acetylcholine at the neuromuscular junction, then there is no signal to initiate and/or continue the action potential (Tortora & Derrickson, 2011). The combination of all of this will cause a degree of flaccidity or paralysis.
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