Neuromuscular junction Essay

When one moves from one position to the other or moves any part of his body it is because of the harmonious contraction and relaxation of the moving muscles. Other movements are carried out by the body cavity and are intrinsic. Example of such movements include sneezing, breathing, urinating defecating and other host of movements. However, muscle movement are as a result of nerve impulses transmitted across the body (Parker, 2013). Movements be studied at several levels of the nervous system. This paper seeks to look and expound on the following event key to movement; Action Potential, Neuromuscular Junction, and Skeletal Muscle Contraction.

Integration, sensation, and response are functions of the nervous system. These functions depend on neurons. Neurons communicate by action potential, which is how changes in a membrane can establish a signal.

The nerve cell membrane at resting state has both the potassium and sodium gates closed. Thus these ions are at an equilibrium concentration. The electric potential inside the cell is -70mV. Though fluctuations in sodium and potassium ions are negligible, the potential is not static. The equilibrium state is maintained by the sodium-potassium ion pump which keeps the high amount of sodium ions outside and the high amount of potassium ion on the inside of the nerve cell.

Upon excitation, the dendrites of the nerve cell receive the stimulus. The sodium ion gates open and there is an inflow of sodium ions to the inside. This drives the inside potential more positive. After the cell reaches the threshold level, the cell drives to full potential. The situation is called the “the all-or-none law”. At the threshold level, sodium ions flood the inside of the cell raising potential speedily. The transition is referred to as the ”voltage-gated” and occurs fast since movement of sodium ions is driven by both the concentration and voltage gradients. The transition drives the inside cell potential from -70mV to about +30mV. The fast transition of the inside cell occurs in the order of milliseconds and is called depolarization.

The open sodium channel gates allow more sodium ions. At some point potassium ion channels start to open on a rather slower pace.  Depolarization continue until +30mV interior potential. The sodium gates then close and depolarization ends. Since potassium ion channels are open, more potassium diffuse out of the cell driving potential to negative. This reverse process is called repolarization. The cell thus becomes negative. When the cells become extremely negative than normal, the situation is called hyperpolarization. Sodium gates remain closed and thus potential proceeds to about -80mV.

Hyperpolarization is vital for information transmission. It also inhibits the neuron from accepting another stimulus. This means an axon cannot receive two or more stimuli at a go either in the same or the opposite direction. The signal thus moves in only one direction.

Under sodium-potassium pump the cell membrane again returns to its rest state/equilibrium. Once action potential is complete, the sodium gates remain briefly closed for a period referred to as ”refractory period”.

The neuromuscular junction is also referred to as the myoneural junction. The junction is where the neuron and the muscle meet. The motor neuron has an axon that sends the signal to the muscle cells. The axon makes contact with different muscle fibers by its branches called synaptic terminals. At the end of the axon, the terminals expand into knobs.  The knobs house many mitochondria and synaptic vessels that contain neurotransmitter acetylcholine (ACh).  A neurotransmitter passes the signal along nerve cells to the muscle cell by changing the permeability of the target muscle cell. The potential flows to the membrane around the synaptic terminal. First, the calcium channels open like gates.  The calcium enters the synaptic vessel. The influx of calcium into the terminal signal the vessels to migrate and fuse with the synaptic terminal. ACh (in the vessels) is released all at once through exocytosism flooding the synaptic cleft.

The ACh binds to the membrane of the receptors on the sarcolemma in the synaptic cleft. The binding causes the membrane potential of the muscle cell membrane to change. The membrane potential is a chemical gradient made up of ion pumps to control sodium and potassium concentration.  The gradient creates a disequilibrium in the ions which in turn create a difference in electrical charges between the inside and outside of the cell. The binding of a neurotransmitter to a cell membrane receptor.rs cause the membrane dynamics to change. This starts a chain reaction along the cell membrane.

The sarcolemma contains membrane receptors on the motor end plate for ACh. The Ach flow across the cleft and bind to the receptors.  A stimulus occurs and once gone, the signal needs to be stopped. The stopping of the signal consists of an enzyme, acetylcholinesterase, that chops ACh into small pieces and recycles it. The enzyme is secreted by muscle cell into the synaptic cleft. Since the concentration of Ach is so high and there is much receptor binding, ACh will be completely broken down. That way contraction is initiated.

A relationship between calcium, sodium, and potassium is accountable for the translation of the action potential to the change in membrane potential and finally cell membrane contraction. Functions such as locomotion, posture, and control of some circulatory systems are performed by the muscular system. This system is made up of muscle tissues and is of three types namely; skeletal, smooth and cardiac.

The skeletal muscle contraction begins when an action potential reaches the synaptic terminal. This causes depolarization of the terminal which induces the opening of the calcium ion gate channels which allows a flux of calcium ions inside the neuron. Increase in the concentration of calcium ions introduces a change in the microtubular section of the synaptic terminal. The changes initiate the exocytotic process in the synaptic vessels which contain ACh neurotransmitter. Through exocytotic ACh is secreted into the postsynaptic cleft towards the sarcolemma. As soon as ACh reaches sarcolemma surface’ it binds with receptors that are ACh specific. The binding between neurotransmitter and receptor initiate changes that allow the opening of the gate channel. The opening, in turn, causes an influx of sodium ions into the muscle fiber. As sodium ions accumulate, depolarization of the membrane occurs giving rise to end plate potential. The potential keeps rising till it achieves an action potential threshold. When the threshold exceeds the positive feedback of sodium ions, the opening allows more of the ions hence ensuring depolarization returns to the normal level which is indicated by an action potential of around +30mV. The action potential spreads through T tubules into the interior of the muscle fibers. The spread of promotes activation of calcium ion-voltage gate channels which open to allow a small influx of calcium ions inside the cell. The small arrival of the calcium ions opens calcium ion gates in the membrane of sarcoplasm reticulum allowing a significant increase in intracellular calcium concentration. The accumulation of calcium ions after the depolarization of skeletal muscle initiate and maintenance contractions of the sarcomere. This means that if the concentration of calcium ions inside the cell is increased, so will the contractile force of the fibers.

In the thin actin filaments, free calcium ions bind with troponin C protein introducing an active calcium-troponin complex. The binding is responsible for the change in troponin C which in turn alter the conformation of the tropomyosin protein. The changes expose actin binding sites where the myosin filaments anchor allowing interactions between thin and thick filaments which altogether elicit contraction.

After the myosin anchors on the exposed binding sites, ADP and Phosphate are released. Power stroke follows, pulling the Z band toward each other.  ATP then binds to myosin- which then detaches from the actin filaments. Myosin hydrolyzes and returns to the cycle until muscle fully contracts.

References

Netter, F. (2015). Atlas of Human Anatomy. Saint Louis: Elsevier Health Sciences.

Parker, S. (2013). The human body book. New York: DK.

Shier, D., Butler, J., Lewis, R., & Hole, J. (2018). Hole’s essentials of human anatomy & physiology. New York, NY.: McGraw-Hill Education.